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DYSPNOEA  AND  CYANOSIS 


DISORDERS   OF 

Metabolism  2sd  Nutrition 

A  Series  of  Monographs 

By  Prof.  Dr.  Cart,  von  Xoorben 

Professor  of  the  First  Medical  Clinic,  Vienna 

I.  Obesity  $   .50 

II.  Nephritis 1.00 

III.  Colitis SO 

I V .  The  Add  Autointoxications 50 

V.  Saline  Therapy 75 

VI.    Drink  Restriction 75 

VII.    Diabetes  Mellitus 1.50 

Complete  Set,  $5.50.    Also  Sold  Singly 

E.  B.  TREAT  &  CO.,  Publishers,  New  York 


CLINICAL    TREATISES 

on  the 

SYMPTOMATOLOGY   and   DIAGNOSIS 

0/  DISORDERS  0/ 
RESPIRATION  w  CIRCULATION 


By  Prof.  Edmund  von  Neusser,  M.D. 

Professor  of  the  Second  Medical  Clinic,  Vienna ;  Associate  Editor 
Nothnagle  's  Practice  of  Medicine 


Authorized  English   Translation 


By  Andrew    MacFarlane,    M,    D., 

Professor  of  Medical  Jurisprudence  and  Physical  Diagnosis, 

Albany  Medical  College;  Attending  Physician  to 

St.    Peter's  and  Child's  Hospital  and 

Albany  Hospital  for  Incurables 


PART  I 
DYSPNCEA  AND   CYANOSIS 


NEW  YORK 

E.     B.     treat      &      COMPANY 

1907 


Copyright,  1907 

by 

E.  B.  TREAT   &  CO., 

New  York 

All  rights  reserved 


PREFACE   TO   AMERICAN    EDITION 

The  development  of  bacteriology  since  Koch's  dis- 
covery of  the  tubercle  bacillus  in  1881,  and  the  applica- 
tion of  solid  culture  media  for  the  differential  growth 
of  bacteria  has  tended  in  the  last  two  decades  to  lead 
the  physician  to  rely  for  his  diagnoses  upon  laboratory 
aids  and  less  upon  clinical  observation.  In  order  to 
be  thoroughly  understood  and  rationally  treated,  dis- 
ease must  be  studied  primarily  in  its  entirety  as  a 
pathological  process.  The  physician  cannot  absolve 
himself  from  this  responsibility  nor  find  any  easy  road 
through  the  work  of  another  to  this  desired  goal. 

The  all-absorbing  search  for  the  specific  cause  of 
a  disease,  although  most  valuable  when  indicated,  has 
too  often  pushed  into  the  background  the  manifest 
clinical  evidences  of  the  disease  and  has  regarded  them 
of  subordinate  value  and  apparently  even  of  negligible 
worth. 

The  diagnosis  of  disease  must  in  the  great  majority 
of  patients  be  determined  at  the  bedside  and  not  in  the 
laboratory.  Laboratory  findings  are  most  valuable 
aids  to  diagnoses,  but  are  not,  except  in  a  few  instances, 
diagnoses  themselves,  and  never  substitutes  for  clinical 
bedside  work. 

This  present  series  of  monographs  accentuates  the 
value  of  the  study  of  symptoms  as  observed  at  the 


6  PREFACE    TO   AMERICAN   EDITION 

bedside  of  the  patient,  and  reproduce  the  marvelous 
clinical  pictures  of  Trousseau,  Niemeyer,  Sydenham, 
Flint  and  others  illuminated  by  present-day  knowledge 
of  pathology  and  clinical  methods. 

Prof.  Edmund  Neusser,  with  his  rare  diagnostic  in- 
stinct and  his  almost  uncanny  memory  of  clinical  facts 
and  their  co-relation  to  pathological  findings,  typifies 
in  the  strict  sense  the  modern  master  clinician. 

These  lectures  are  the  resultant  of  an  almost  limit- 
less clinical  material  and  of  a  scientific  acumen  which 
does  not  overlook  any  fact  no  matter  how  seemingly 
trivial  and  unimportant. 

Andrew  MacFarlane. 


CONTENTS 


PART  I 

DYSPNCEA  AND   CYANOSIS   IN  DISORDERS  OF 
THE  RESPIRATION 

CHAPTER  PAGE 

I.  Conditions  which  Induce  Dyspncea         .  17 

Deficiency  of  Oxygen  or  Excess  of  Car- 
bon Dioxid,  the  Cause  of  Dyspnoea     .  18 

Clinical       Dyspnoea       Accompanied       by 

Cyanosis        20 

Absence    of    Dyspnoea    and    Cyanosis    in 

Many  Disturbances  of  Respiration     .  22 

Cyanosis  without  Dyspnoea       ....  24 

II.  Dyspncea   and   Cyanosis   in   Diseases   of 

THE  Respiratory  Tract       ....  26 

Respiratory  Tract  (Nose  and  Pharynx)    .  26 

Laryngeal  Affections 2y 

Diseases  of  the  Trachea 34 

Goitre         35 

Affections  of  the  Bronchi 2>7 

Bronchial  Asthma 40 

Pertussis          ,  47 

Fibrinous  and  Capillary  Bronchitis      .      .  48 

Pneumonia 51 

Hyperemia  of  the  Lungs 55 

Edema  of  the  Lungs 56 

Pulmonary  Emboli  and  Thrombi     ...  57 

Gangrene        ., 61 

9 


lO  CONTENTS 

CHAPTER  PAGE 

Pulmonary  Emphysema 6i 

Atrophy  and  Contraction  of  the  Lungs  66 

Pulmonary  Syphilis  and  Actinomycosis     .  68 

Tumors  of  the  Lung  and  Bronchi    ...  69 

Tuberculosis          71 

Pleural   Exudates          79 

Pneumothorax,  Pyo-pneumothorax      .      .  83 

Scoliosis          85 


PART  11 

DYSPNCEA  AND    CYANOSIS   IN   DISORDERS 
OF  THE   CIRCULATION 

I.  Dyspncea   and   Cyanosis   in    Congenital 

Cardiac  Defects 87 

Stenosis    of   the    Pulmonary    Artery   and 

Insufficiency  of  the  Tricuspid       .      .  94 

Open  Foramen  Ovale 94 

Open  Ductus  Arteriosus 95 

Stenosis  of  the  Aorta 95 

Transposition  of  the  Large  Vessels     .  96 

Mitral  Stenosis   (Congenital)          ...  97 

IL  Dyspncea  and  Cyanosis  in  Acquired  Car- 
diac Lesions         100 

Mitral  Insufficiency  and  Stenosis         .      .  100 

Aortic  Lesions 100 

Affections  of  the  Pulmonary  Valve      .      .  loi 

Acute  Ulcerative  Endocarditis        .     .      .  loi 

Purulent  Aortitis 103 

Pericarditis  and  Adhesive  Pericarditis       .  104 

Hydro-,  Hemo,-  and  Pneumo-Pericardium  106 

Fatty  and  Muscular  Degenerations       .      .  108 

Thrombosis  of  the  Heart ,110 


CONTENTS  1 1 

CHAPTER  PAGE 

Theories   of   Cardiac    Dyspnoea    (Basch's 

and  Fraenkel's) iii 

Final  Cause  of  Cardiac  Dyspepsia       .      .  113 

Dyspnoea  and  Blood  Pressure        .      .      .  115 

III.  Dyspnoea    and    Cyanosis    in    Vascular 

Lesions 116 

Arteriosclerosis  and  Anemia  .  .  .  .  116 
Arteriosclerosis  and  Pseudo-anemia  .  .  116 
Arteriosclerosis  and  the  Heart  .  •  .  117 
Arteriosclerosis  and  the  Kidneys  .  .  .  122 
Cerebral  and  Spinal  Arteriosclerosis  .  .  124 
Significance  of  Dyspnoea  in  Arterio- 
sclerosis            124 

Aneurism  of  the  Aorta         127 

Aneurism  and  Sclerosis  of  the  Pulmonary 

Artery 129 

IV.  Dyspnoea  and  Cyanosis  in  Neuroses  of 

THE  Heart 131 

Cardiac  Asthma 131 

Paroxysmal  Tachycardia 132 

V.  Dyspncea  and   Cyanosis   in   Diseases   of 

the  Gastro-intestinal  Tract       .      .  134 

Diseases  of  the  Stomach 134 

Diseases  of  the  Liver  and  Gall-bladder  .  134 

VI.  Dyspncea    and    Cyanosis    in    Infectious 

Diseases 137 

Diphtheria 138 

Measles,  Scarlet  Fever,  and  Variola       .  138 

Malaria 139 

Typhoid,   Typhus,  Relapsing  Fever    .      .  141 

Erysipelas,  Influenza 141 

Plague 142 


12  CONTENTS 

CHAPTER  PAGE 

Anthrax 142 

Malignant  edema 143 

Glanders           144 

Trichinosis 144 

Asiatic  Cholera,  Peritonitis       ....  145 

VII.  Dyspncea  and  Cyanosis  Due  to  Poisons  .  148 

Morphin,  Chloroform,  Alcohol,  Tobacco  148 
Belladonna,    Hyoscyamus,    Calabar   Bean, 

Physostigmin,  Aconite,  Colchicum     .  149 

Strychnin,  Camphor,  Curare,  Conium       .  150 

Tetroden  Fish,  Fungus,  Agaric  Gnat     .  151 

Barium  Salts,  Corrosive  Substances     .      .  152 

Irritating  Gases  and  Vapors     ....  153 

Digitalis,  Hellebore  and  Veratrum      .      .  154 

Phosphorus           154 

Carbon  Monoxid 154 

Substances  Forming  Methemoglobin  .      .  156 

Antipyrin,  Benzol  Derivatives,  Acetanilid  157 
Nitroglycerin,  Amyl   Nitrit  and   Carbolic 

Acid          158 

Arseniated     Hydrogen     and     Potassium 

Chlorat          159 

Nitrits — Sodium  and  Potassium     .      .      .  160 

Nitrous  Acid,  Prussia  Acid       ....  162 

Sulfuretted  Hydrogen          164 

Botulism,     Tetanus      Toxin,      Poisonous 

Fish          165 

Insect  Stings,  Snake  Bites         ....  166 

Beri-beri,  Anesthetic  Leprosy         .      .      .  167 

VIII.  Dyspncea  and  Cyanosis  in  General  Dis- 
eases        169 

Bright's  Disease         ,  169 

Chronic  Nephritis 170 


CONTENTS  13 

CHAPTER  PAGE 

Contracted  Kidney,  Cystic  Kidney       .      .  170 

Renal  Asthma  versus  Cardiac  Asthma      .  171 

Latent  Nephritis         172 

Hemoptysis  in  Contracted  Kidney       .      .  173 

Cyanosis  of  Uremia 174 

Reduced  Hemoglobin  in  Blood     .      .      .  174 

Diabetes           175 

Cyanosis  in  Diabetes 176 

Hydrophobia         177 

Anemia 179 

Leukemia         180 

Absence  of  Cyanosis  in  Anemia     .      .      .  181 

Polycythemia 183 

Asthma  Dyspepticum 184 

Hysteria  and  Neurasthenia       .      .     .      .  187 
Type  of  Hysterical  Dyspnoea    .      .      .      .  188 
Disturbances    of   Respiration    in    Neuras- 
thenia         192 

Reflex  Asthma 193 

Organic  Cerebral  Lesions 193 

Organic  Spinal  Lesions ,  194 

Neuritis 195 

Myositis           198 

IX.  Therapy  of  Dyspncea 200 


PART    I 

DYSPNOEA   AND    CYANOSIS    IN    DIS- 
ORDERS OF  THE  RESPIRATION 


CONDITIONS  WHICH  INDUCE  DYSPNCEA 

Limitation  in  the  interchange  of  gases  between 
the  blood  and  the  atmospheric  air  causes  an  accumu- 
lation of  carbon  dioxid  and  a  deficiency  of  oxygen 
in  the  blood.  Both  factors  act  as  irritants  to  the 
motor  center  of  respiration,  inciting  the  latter  to  in- 
creased activity.  This  disturbance  when  marked  gives 
rise  to  the  subjective  sensation  of  air  hunger,  or 
dyspnoea,  which  is  felt  the  more  keenly,  the  greater 
the  demand  for  oxygen  becomes  in  the  tissue  cells. 
Dyspnoea,  therefore,  occurs  in  all  cases  in  which  the 
interchange  of  gases  is  obstructed,  by  depriving  the 
blood  of  its  supply  of  air,  as  in  laryngeal  and  tracheal 
stenosis ;  by  a  restricted  area  of  respiration,  as  in  affec- 
tions of  the  bronchi  and  lungs ;  or  by  reduced  elasticity 
of  the  lungs.  When  pulmonary  stasis  and  diminished 
power  of  circulation,  as  in  cardiac  insufficiency,  in- 
terfere with  the  supply  of  blood  to  the  respired  air 
in  the  lungs,  or  when  inability  of  the  blood  to  absorb 
the  oxygen  and  transmit  it  to  the  tissues,  as  may  be  the 
case  in  intoxications  (carbon  monoxid),  dyspnoea 
results. 

As  is  well  known,  the  arterialization  of  the  venous 
blood  by  oxydation  and  decarbonization  is  effected  by 

17 


1 8         DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

the  blood  absorbing  oxygen  from  the  air  and.  giving 
up  the  carbon  dioxid.  This  interchange  of  gases 
takes  place  in  accordance  with  the  laws  of  gas  dif- 
fusion by  equalization  of  tension.  Bohr's  assumption 
that  this  migration  of  gases  is  assisted  by  a  vital  re- 
action or  a  gas  secretion  in  which,  under  the  influence 
of  the  nerves,  oxygen  is  positively  sucked  up  and  car- 
bon dioxid  expelled,  is  not  sufficiently  free  from  objec- 
tions to  be  acceptable  without  further  investigation. 
It  is  certainly  a  tempting  theory  to  look  upon  the  lungs 
as  a  gas-secreting  gland  acting  under  the  influence  of 
the  nervous  system.  The  importance  of  the  latter,  and 
especially  that  of  the  vagus,  would  then  appear  in  a 
new  light,  so  far  as  the  regulation  of  respiration  is  con- 
cerned. 

DEFICIENCY  OF  OXYGEN  OR  EXCESS   OF   CARBON 
DIOXID^   THE   CAUSE   OF  DYSPNCEA 

Although  it  is  admitted  that  dyspnceic  respiration 
is  incited  by  insufficiency  of  oxygen  and  excess  of  car- 
bon dioxid  in  the  blood,  it  is  an  open  question  whether 
the  first  or  the  second  is  the  main  factor  in  producing 
irritation  of  the  medulla  oblongata.  Physiologists  do 
not  agree  as  to  whether  the  activity  of  the  respiratory 
center  is  regulated  by  oxygen  or  carbon  dioxid. 
Pfliiger  states  that  marked  dyspnoea  can  arise  when 
oxygen  is  deficient,  even  if  the  quantity  of  carbon  di- 
oxid" in  the  blood  is  diminished.  On  the  other  hand, 
dyspnoea  occurs,  even  when  there  is  an  excess  of  oxy- 
gen, as  soon  as  the  carbon  dioxid  tension  exceeds  the 


DYSPNCEA   AND   CYANOSIS  1 9 

normal.  Carbon  dioxid  has  been  found  to  undergo  in 
the  arterial  blood  of  the  woodchuck  during-  hiberna- 
tion an  increase  up  to  76%  without  causing  dyspnoea. 
It  is  conceded,  however,  that  this  animal  is  hyposensi- 
tive. 

It  will  be  seen,  therefore,  that  an  overcharge  of  the 
blood  with  carbon  dioxid  may  be  borne  very  well,  and 
that  the  influence  it  exerts  upon  the  regulation  of  the 
respiratory  function  is  not  yet  definitely  established. 
At  the  same  time  the  diminution  of  the  oxygen  tension 
of  the  blood  as  a  respiratory  irritation  is  likewise  a 
debatable  point.  Although  the  majority  of  observers 
attribute  the  dyspnoea  of  aeronauts  and  mountaineers 
to  diminished  tension  of  oxygen  and  insufficient  satura- 
tion of  the  hemoglobin  with  oxygen,  others,  for  in- 
stance Mosso,  explain  the  so-called  mountain  sickness 
by  a  decrease  of  carbon  dioxid  in  the  blood,  caused  by 
accelerated  evaporation  in  the  rarefied  air,  which  pre- 
vents the  normal  excitation  of  the  respiratory,  cardiac 
and  vascular  centers. 

Deficiency  of  oxygen  and  excess  of  carbon  dioxid 
are  therefore  both  of  importance  in  the  causation  of 
dyspnoea.  The  asphyxia  of  the  newborn,  of  people 
working  in  cellars  filled  with  gas,  or  of  dogs  in  the 
grotta  del  cane  near  Naples,  may  be  laid  to  both. 

Insufficiency  of  oxygen  causes  dyspnoea  if  it  occurs 
suddenly  and  attains  a  high  degree;  gradual  diminu- 
tion of  oxygen  alone  does  not  cause  dyspnoea,  as 
demonstrated  by  the  experiments  of  Zuntz  and  Lowy, 
A  slight  increase  in  carbon  dioxid,  however  (even  with 


20         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

excess  of  oxygen),  causes  a  distinct  increase  in  respira- 
tions. Under  pathological  conditions,  at  the  bedside, 
both  factors — deficiency  of  oxygen  and  accumulation 
of  carbon  dioxid — are  nearly  always  to  be  considered, 
especially  in  sudden  disturbances  of  respiration,  as 
in  acute  stenoses  of  the  upper  air  tract.  In  slowly 
developing  respiratory  difficulties,  the  accumulation  of 
carbon  dioxid  in  the  blood  should  be  held  primarily 
responsible,  while  deficient  oxygen  probably  plays  a 
subsidiary  role. 

The  change  in  the  gaseous  composition  of  the  blood 
is  the  cause  of  dyspnoea  in  the  majority  of  patholog- 
ical conditions.  It  may,  however,  also  be  due  to  other 
causes,  either  abnormal  irritation  of  the  respiratory 
center,  or  because  the  latter  is  In  a  state  of  hyperex- 
citability.  Thus,  for  example,  dyspnoea  is  found  with 
high  temperature,  after  excessive  muscular  efforts,  in 
acid  intoxications,  in  organic  and  functional  nervous 
diseases.  In  some  cases,  toxic,  easily  oxydizable  sub- 
stances may  play  a  part,  analogous  to  the  products  of 
fatigue,  which  accumulate  in  the  tissues  in  conse- 
quence of  oxygen  deficiency  and  act  as  an  irritant  upon 
the  center  of  respiration. 

CLINICAL  DYSPNCEA   ACCOMPANIED  BY   CYANOSIS 

At  the  sickbed  dyspnoea  is  usually  accompanied  by 
a  second  symptom,  cyanosis.  Formerly  cyanosis  was 
regarded  as  a  result  of  increased  carbon  dioxid  in 
the  blood,  but  to-day  it  is  recognized  that  the  differ- 
ences in  color  between  the  arterial  and  venous  blood 


DYSPNCEA   AND   CYANOSIS  21 

are  not  occasioned  by  the  carbon  dioxid,  but  by  a 
changed  percentage  of  oxygen,  and  that  the  blue  color 
of  the  peripheral  veins  is  attributable  to  interference 
with  light  rays  in  the  skin. 

Both  experimental  and  clinical  observations,  espe- 
cially in  intoxications  from  methemoglobin-forming 
substances,  demonstrate  that  cyanosis,  so  far  as  it 
depends  on  the  quantity  of  gas  contained  in  the 
blood,  may  occur  independently  of  carbon  dioxid  satu- 
ration. The  fact,  however,  that  in  the  great  majority 
of  cases  there  actually  is  an  excess  of  carbon  dioxid,  is 
explained  by  the  decreased  elimination  of  carbon 
dioxid  from  insufficient  respiratory  function,  in  dis- 
turbances of  the  respiratory  apparatus,  and  also  in 
affections  of  the  organs  of  circulation. 

Divers,  after  remaining  under  water  for  some 
minutes,  return  to  the  surface  in  a  markedly  cyanotic 
state,  occasioned  in  all  probability  by  both  insufficiency 
of  oxygen  and  excess  of  carbon  dioxid.  The  primary 
cause  of  the  cyanosis,  however,  is  the  consumption  of 
the  circulating  oxygen. 

The  flooding  of  the  organism  with  oxygenated  blood 
depends  upon  the  quantity  of  blood  circulating  in  a 
given  unit  of  time.  The  rapidity  of  the  circulation  of 
the  blood  is  influenced  by  the  quantity  of  blood  thrown 
out  by  the  heart  into  the  vessels,  and  also  by  the  resist- 
ance against  which  the  blood  is  expelled.  With  di- 
minished motor  power  and  abnormal  increase  of 
resistance,  the  flooding  of  the  organism,  and  thereby 
the  oxygen  supply,  must  suffer.     The  diminution  of 


22        DISORDERS     OF     RESPIRATION   AND   CIRCULATION 

the  vis  a  tergo  may,  therefore,  by  retardation  of  the 
circulation,  lead  to  consumption  of  the  oxygen  trans- 
mitted with  the  arterial  blood  to  the  capillaries,  and 
thus  cause  a  reduction  to  the  minimum  of  the  oxygen 
supply  in  the  venous  blood  flowing  from  the  tissues. 
A  similar  effect  may  also  be  produced  by  an  abnormal 
reduction  of  the  resistance  in  consequence  of  dilatation 
of  the  abdominal  vessels.  Owing  to  the  reduction  of 
pressure  in  the  aortic  system,  the  organs  do  not  receive 
a  sufficient  supply  of  blood  and  become  impoverished 
in  oxygen,  which  gives  rise  to  conditions  of  collapse, 
as  in  peritonitis  and  partly  also  in  cholera.  This  ac- 
cumulated venous  blood,  deprived  of  oxygen  and 
enriched  with  carbon  dioxid,  causes  the  cyanotic  colora- 
tion of  vascular  and  transparent  parts  of  the  body.  It 
can  attain  a  high  degree  of  intensity  from  increased 
venous  pressure,  especially  from  obstructed  flow  of  the 
venous  blood  due  to  insufficient  aspiratory  action  of 
the  right  heart.  Therefore,  not  only  the  chemical  fac- 
tors of  diminished  arterialization  of  the  pulmonary 
blood  and  increased  venosity  of  the  capillary  blood,  but 
also  the  mechanical  factor  of  the  congested  venous 
system  of  the  general  and  pulmonic  circulations  par- 
ticipate in  the  causation  of  dyspnoea  and  cyanosis. 

ABSENCE  OF  DYSPNCEA  AND  CYANOSIS  IN  MANY 
DISTURBANCES  OF  RESPIRATION 

Frequently,  however,  in  extensive  pleuritic  exudates, 
incapacitating  an  entire  lung,  or  in  extensive  destruc- 
tion of  the  pulmonary  parenchyma,  there  is  neither 


DYSPNCEA   AND    CYANOSIS  23 

dyspnoea  nor  cyanosis,  provided  patients  stay  quietly 
in  bed.  The  consumption  of  oxygen  is  thus  limited 
to  the  lowest  point  and  the  muscular  activity  confined 
to  the  minimum.  Should,  however,  the  need  of 
oxygen  be  suddenly  increased  by  a  diminution  of 
the  respiratory  surface  or  by  the  occurrence,  from 
various  causes,  of  an  increased  demand  for  oxygen  in 
the  organism,  dyspnoeic  respiration  will  manifest  itself. 
Dyspnoea,  therefore,  acts  like  a  regulator,  by  which  the 
organism  defends  itself  against  the  impending  im- 
poverishment of  oxygen.  In  deeper  respirations  the 
pressure  of  oxygen  in  the  alveoli  is  increased,  with 
the  result  that  the  pulmonary  blood  absorbs  a  greater 
quantity  of  oxygen.  This  reinforced  respiratory  action 
assists  in  the  evacuation  of  the  blood  from  the  periph- 
eral veins  to  the  heart;  the  blood  stream  is  acceler- 
ated, which  also  aids  in  providing  the  blood  with  more 
oxygen  and  in  depleting  it  of  carbon  dioxid.  It  is 
only  after  failure  to  re-establish  the  normal  gas-com- 
position of  the  blood  in  spite  of  assisted  aeration  of 
the  lungs,  that  the  venosity  of  the  blood  increases  and 
cyanosis  occurs  in  consequence  of  deficient  oxygen. 
In  due  course  the  body  becomes  cold ;  there  is  drowsi- 
ness; subjective  dyspnoea  disappears  in  consequence  of 
insensibility  of  the  brain;  respirations  become  more 
frequent  and  superficial,  until  finally  asphyxia  sets  in, 
which,  by  stopping  the  heart's  action,  leads  to  death 
as  soon  as  the  organs  are  no  longer  excitable  owing  to 
the  deficiency  of  oxygen. 

In  disturbances  of  the  respiratory  apparatus  with 


24         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

dyspncea.  pronounced  cyanosis  therefore  only  occurs 
when  the  respiration  is  not  strong  enough  to  arteri- 
alize  the  blood  through  increased  pulmonary  action. 
The  cause  of  this  may  be  that  the  impediment  to  respi- 
ration is  too  great  at  the  outset,  or  that  the  respiratory 
muscles  and  their  innerv^ation  are  too  weak  either 
from  the  first  or  have  become  weakened  in  their  effort 
to  overcome  the  obstruction  to  respiration.  For  this 
reason  the  improvement  of  a  previously  existing 
dyspnoea  with  the  simultaneous  appearance  or  intensi- 
fication of  cyanosis,  is  an  indication  of  respiratory 
insufficiency,  and,  therefore,  as  a  rule,  a  prognostically 
ominous  manifestation  in  disturbances  of  respiration. 

CYANOSIS    WITHOUT    DYSPNCEA 

On  the  other  hand,  sometimes  in  deep  cyanosis,  as 
for  instance  in  congenital  cardiac  deficiency,  there  is 
an  absence  of  all  disturbances  of  respiration,  even  with 
increased  muscular  work.  Owing  to  the  absence  of 
dyspnoea  there  is  no  reaction  and  the  supply  of  oxygen 
to  the  tissues  and  its  consumption  must  be  regulated 
in  a  different  manner.  Rapidity  of  circulation  due 
to  compensatory  hypertrophy  of  the  heart,  increase  of 
the  hemoglobin,  polycythemia,  concentration  of  the 
blood  by  transudation  of  plasma,  may  represent  the 
regulating  forces  employed  by  the  organism  to  defend 
itself  against  the  deficiency  of  oxygen.  It  is  possible 
also  that  the  organism  deteriorates  by  becoming 
accustomed  to  the  deficiency  of  oxygen,  and  the  respi- 
ratory center  sacrifices  its  excitability  to  the  increased 
venosity  of  the  blood. 


DYSPNCEA   AND    CYANOSIS  2$ 

It  is  therefore  possible  that  even  in  extensive  respira- 
tory obstruction  both  dyspnoea  and  cyanosis  may  be 
absent,  and  that  in  cases  where  both  symptoms  are 
present  they  do  not  always  follow  a  parallel  course  in 
that  dyspnoea  preponderates  in  disturbances  of  respira- 
tion and  cyanosis  in  those  of  the  circulation.  Then, 
too,  there  are  cases  of  prolonged  dyspnoea  without 
cyanosis.  This  refers  especially  to  those  affections 
in  which  disturbance  of  respiration  is  due  to  direct 
or  reflex  excitation  of  the  central  nervous  organs  of 
the  respiratory  system.  It  is  frequently  observed  in 
the  dyspnoea  with  high  temperature,  in  the  heavy 
breathing  which  precedes  coma  diabeticum,  and  in 
bronchial  asthma.  In  other  cases  the  clinical  picture  is 
varied  by  extreme  pallor  instead  of  cyanosis.  This 
may  occur  In  the  initial  stage  of  hydrophobia,  or  in 
cases  where  from  various  causes  anemia  is  present, 
as  in  internal  hemorrhage,  perforating  aneurisms,  and 
in  penetrating,  shooting  and  stab  wounds. 


II 

DYSPNOEA   AND   CYANOSIS   IN    DISEASES 
OF   THE   RESPIRATORY   TRACT 

UPPER   RESPIRATORY   TRACT    (nOSE   AND   PHARYNX ) 

In  affections  of  the  nose,  dyspnoea  has  been  observed 
to  reach  such  a  degree  as  to  assume  the  character  of 
orthopnoea.  The  troublesome  breathing,  during  nurs- 
ing, of  the  newborn,  who  suffer  from  (syphihtic) 
coryza,  is  explained  by  the  obstructed  nasal  ducts.  The 
dyspnoea  forces  the  infant  to  interrupt  the  act  of  nurs- 
ing, and  if  this  continues  sufficiently  long,  there  may  be 
exhaustion  and  even  fatal  termination  owing  to  inabil- 
ity to  take  nutrition.  Independently  of  nursing,  dysp- 
noeic  manifestations  may  occur  in  coryza,  severe 
enough  to  assume  the  character  of  orthopnoea.  These 
paroxysms  are  explained  by  the  great  irritability  of 
the  nasal  mucous  membranes  and  the  prevalence  of 
nasal  breathing  in  the  newborn. 

In  adults  with  unilateral  nasal  stenosis,  there  may 
be  dyspnceic  paroxysms  at  night,  especially  if  patients 
lie  on  the  side  opposite  to  the  stenosis.  Lermoyez  ob- 
served an  hysterical  girl  of  fifteen  who  was  unable  to 
breathe  through  the  nose,  although  the  ducts  were  per- 
meable. Upon  covering  the  mouth  with  the  hand, 
there  was  immobilization  of  the  thorax  with  manifes- 
tations of  dyspnoea. 

Foreign  bodies,  especially  large  pieces  of  badly  mas- 

26 


DYSPNCEA   AND    CYANOSIS  2'y 

ticated  food,  may  stick  in  the  faucial  isthmus,  causing 
the  danger  of  suffocation  and  cyanosis.  In  this  con- 
nection a  case  observed  by  me  is  interesting.  There 
was  a  sudden  attack  of  deep  cyanosis  and  dyspnoea,  due 
to  a  uvular  cyst  (herpes  uvulce),  filled  v^ith  bloody- 
serous  fluid,  the  size  of  a  plum  and  obstructing  the 
faucial  isthmus.  After  the  cyst  was  punctured  and 
emptied,  all  the  threatening  manifestations  instantly 
disappeared.  Hinsdale  described  a  case  of  universal 
urticaria  with  deep  dyspnoea,  caused  by  edematous 
swelling  of  the  uvula.  Evidently  the  urticaria  had 
become  localized  in  the  soft  palate,  and  an  application 
of  cocaine  soon  removed  the  trouble.  Similar  swell- 
ings have  been  observed  in  pemphigus  and  multiform 
exudative  erythema. 

LARYNGEAL  AFFECTIONS 

Cyanosis  with  difficulty  in  breathing  is  a  frequent 
symptom  in  affections  of  the  larynx,  caused  by  acute 
or  chronic  constrictions  or  occlusions  of  the  respira- 
tory tract.  In  laryngeal  dyspnoea,  the  mechanical  im- 
pediment to  breathing  is  usually  complicated  by  a  spas- 
modic symptom,  spasm  of  the  glottis.  This  spasm 
occurring  in  children  is  sufficient  to  produce  mani- 
festations of  suffocation  and  cyanosis  as  takes  place 
in  tetany,  eclampsia  and  in  complications  of  simple 
laryngitis,  also  in  inflammations  of  adenoid  vegeta- 
tions and  in  the  presence  of  foreign  bodies.  In  these 
cases  both  voice  and  respiration  are  perfectly  nor- 
mal in  the  aspastic  intervals.  In  adults,  laryngo- 
spasm,  as  it  occurs  in  epilepsy,  tetany,  paramyoclonus, 


28         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

chorea,  hydrophobia  and  tabes,  also  in  cerebral  tumor 
and  hydrocephalus,  is,  as  a  rule,  less  stormy. 

In  the  pseudo-croupous  form  of  catarrhal  laryngitis, 
the  spastic  element  is  to  be  considered  in  addition  to 
the  inflammatory  swelling  of  the  mucous  membrane. 
As  the  spasm  relaxes,  there  are  almost  entirely  free 
intervals,  while  in  genuine  croup  the  mechanical  im- 
pediment predominates  and  the  dyspnoea  remains  per- 
manent, as  the  spastic  element  is  not  an  important  factor 
in  consequence  of  the  paralysis  of  the  musculature  of 
the  glottis.  In  very  severe  laryngitis  with  inflamma- 
tory edema  below  the  vocal  cords  (laryngitis  subglot- 
tica),  difficulty  of  respiration  may  persist  even  in  the 
inter\'als  between  the  dyspnoeic  paroxysms.  The  voice 
becomes  coarse  as  in  pseudo-croup,  but  not  so  husky 
and  hoarse  as  in  genuine  croup. 

Dyspnoea  with  paroxysms  of  suffocation  and  pain- 
ful oppression,  incessant  violent  irritation  to  coughing, 
occurs  in  measles,  partly  in  consequence  of  the  fol- 
licular swelling  which  accompanies  the  catarrh  in 
measles,  in  part  as  a  result  of  the  inflammatory  edema 
of  the  subglottic  zone,  and  partly  from  ulceration  and 
erosion  of  the  laryngeal  mucous  membrane.  Some- 
times these  grave  laryngeal  symptoms  occur  in  the  pro- 
dromal stage,  and  Hebra  in  his  lectures  mentioned 
cases  which  had  been  transferred  to  the  surgical  di- 
vision for  tracheotomy  and  in  the  further  course  turned 
out  to  be  suffering  from  measles.  It  is  a  question  of 
prodromal  exanthema  of  the  larynx,  and  as  the  exan- 
thema appears  on  the  body,  dyspnoea  rapidly  disap- 


DYSPNCEA   AND   CYANOSIS  29 

pears.  Cases  in  which  genuine  croup  with  diphtheria 
bacilli  occur  as  complication  of  measles  must  be  dif- 
ferentiated. The  difficulties  of  respiration  show  here 
a  progressive  character. 

In  rare  cases  varicella  may  produce  manifestations 
of  suffocation  if  the  process  becomes  located  in  the 
larynx.  Marfan  and  Halle  have  described  such  cases. 
The  diagnosis  may  give  rise  to  difficulty  in  case 
the  larynx  Is  Involved  before  the  eruption  of  the 
exanthema.  In  typhoid  fever,  also,  laryngeal  symp- 
toms may  occupy  a  prominent  place  at  an  early  stage, 
especially  In  children  (laryngo-typhold). 

The  usual  picture  of  stenosis  of  the  respiratory  tract 
is  well  known.  The  difficulty  in  breathing  occurs 
especially  In  inspiration,  while  expiration,  particularly 
the  cough,  Is  suppressed  as  much  as  possible.  In  chil- 
dren suffering  from  croup  the  voice  becomes  hoarse 
and  aphonic,  as  does  the  cough.  Orthopnoea  occurs, 
and  If  the  attacks  are  frequent,  there  is  persistent 
cyanosis.  Inspiration  is  protracted.  Increased  by  the 
auxiliary  muscles  of  inspiration  and  accompanied  by 
loud  stridor.  Downward  movement  of  the  larynx,  in- 
spiratory retraction  of  the  intercostal  spaces,  fossa 
jugularls,  supraclavicular  fossae  and  epigastrium, 
stenotic  breath  sounds,  diminution  or  entire  absence 
of  vesicular  respiration,  are  characteristics  of  a  sten- 
otic attack.  Expiration  likewise  is  obstructed  in  croup, 
protracted  and  noisy,  and  the  great  effort  of  all  the 
auxiliary  muscles  of  expiration,  which  serve  to  con- 
tract the  thorax,  is  evident.     The  expiratory  effort 


30         DISORDERS   OF   RESPIRATION   AND  CIRCULATION 

alone,  by  which  the  blood  is  expressed  from  the 
thorax,  also  the  inspiratory  insufficiency  of  aspiration, 
may  cause  cyanosis  with  dilatation  of  the  cervical  veins. 
The  effect  of  croupous  dyspnoea  is  therefore  double,  as 
stenosis  interferes  with  both  inspiration  and  expira- 
tion. 

In  most  cases  of  laryngeal  stenosis  the  inspiratory 
type  preponderates.  The  prototype  of  this  form  of 
dyspnoea  is  considered  to  be  paralysis  of  the  posterior 
cricoarytenoid  muscles,  which  may  be  the  only  expres- 
sion of  a  tabes  for  some  length  of  time.  The  difficulty 
in  breathing  occurs  particularly  in  great  muscular  exer- 
tions and  is  accompanied  by  loud  stridor  with  unob- 
structed expiration  and  normal  phonation. 

Polypi  above  the  glottis  usually  cause  inspiratory 
dyspnoea,  especially  when  patients  take  a  posture 
opposite  the  site  of  the  polypus.  The  pedunculated 
tumor  obstructs  the  glottis,  while  forced  inspiration 
only  serves  to  render  the  occlusion  of  the  rima  still 
more  complete.  Polypi  below  the  glottis  may  obstruct 
the  latter  at  expiration  like  a  valve,  thereby  causing 
expiratory  dyspnoea  with  normal  and  unimpeded  in- 
spiration. Laryngeal  polypi  develop  slowly  with 
progressive  disturbances  in  phonation.  Sometimes, 
however,  they  may  produce  sudden  attacks  of  asphyxia 
which  require  immediate  surgical  interference. 

Paralysis  of  the  glottic  muscles  in  affections  of  the 
pneumogastric  nerve,  in  cerebral  hemorrhages,  in 
emboli  of  the  vertebral  artery,  hydrocephalus,  nuclear 
paralysis  of  the  vago-accessorius,  compression  of  the 


DYSPNCEA   AND   CYANOSIS  3 1 

oblongata  through  tumors,  pressure  on  the  pneumo- 
gastric  nerve  by  contractures,  aneurisms  of  the  carotid, 
metastatic  swelHngs  about  the  neck  and  jugular  fora- 
men, abscesses  and  tumors,  ascending  inflammations 
of  the  neck  from  pathological,  mediastinal  conditions ; 
furthermore  degeneration  of  the  pneumogastric  nerve 
as  occurs  in  tabes,  amyotrophic  lateral  sclerosis  and  in 
neuritis  of  the  pneumogastric  nerve  (lead  poisoning, 
alcoholism,  beri-beri,  typhoid,  etc.)  :  all  these  con- 
ditions cause  dyspnoea  and  cyanosis.  Similar  effects 
may  be  produced  by  myopathic  processes  of  the  glottic 
muscles,  as  for  instance  after  lues,  diphtheria  and  tri- 
chinosis. 

Dyspnoea  and  cyanosis  from  laryngeal  edema  is  met 
with  in  renal  and  cardiac  affections,  goitre,  amyloidosis 
of  the  organs,  acute  laryngitis — especially  its  phleg- 
monous form — perichondritis,  especially  of  the  aryte- 
noid cartilages,  ulcers  of  the  larynx,  syphilis  and  lepra ; 
also  in  inflammatory  processes  of  the  tongue,  palate 
and  tonsils,  less  often  of  the  parotid,  submaxillary 
glands  and  the  thyroid,  in  carcinoma  of  the  esophagus 
and  aneurism  of  the  aorta.  Laryngeal  catarrh  which 
attacks  pregnant  women  or  had  existed  before  preg- 
nancy, may  lead  to  serious  dyspnoea  and,  if  complicated 
by  laryngeal  edema,  to  death.  Dyspnoea  in  edema  of 
the  glottis  is  chiefly  Inspiratory,  because  the  aryepiglot- 
tlc  folds  close  down  like  valves,  and  open  up  again  at 
expiration.  This,  however,  presupposes  a  certain 
mobility  of  the  folds.  If  the  Infiltration  be  tense,  the 
dyspnoea   will   make    itself    felt   in   both    respiratory 


32         DISORDERS   OF  RESPIRATION  AND  CIRCULATION 

phases.  The  voice  in  these  conditions  is  usually  lit- 
tle changed,  unlike  croup,  where  hoarseness  prevails. 

Angioneurotic  laryngeal  edema  belongs  in  this 
group,  also  those  rare  cases  which  are  regarded  as 
urticaria  of  the  larynx;  and  finally  edema  occurring 
from  the  use  of  iodin.  Marfan  and  Sevestre  record 
the  recurrence  of  stenotic  symptoms  after  injections  of 
antidiphtheritic  serum,  a  phenomenon  similar  to  the 
serum  exanthema,  and  caused  by  the  edematous  swell- 
ing of  the  laryngeal  mucous  membrane,  and  therefore 
a  sequel  of  the  primary  affection. 

In  poisoning  with  corrosive  substances,  in  scalds,  in 
typhoid,  scarlet  fever,  erysipelas,  pyemia,  glanders 
and  ulcerative  endocarditis,  dyspnoea  is  not  a  rare  con- 
comitant manifestation.  In  the  course  of  these  affec- 
tions, edema  of  the  glottis  may  occur  owing  to  ulcer- 
ation and  inflammation  of  the  submucous  cellular  tissue 
or  to  perichondritis. 

In  typhoid  fever,  the  appearance  of  dyspnoea  with 
great  hoarseness,  pain  in  the  larynx,  cough,  occasion- 
ally dysphagia,  should  even  at  an  early  stage  of  the 
disease  direct  attention  to  ulcerative  perichondritis. 
Also  in  the  later  course  of  typhoid  in  the  fifth  and 
even  up  to  the  eighth  week  laryngeal  edema  may  occur 
and  the  stenosis  may  cause  such  an  intense  degree  of 
dyspnoea  that  tracheotomy  is  necessary  to  save  the 
patient's  life. 

In  Ludwig's  angina,  dyspnoea  may  be  occasioned 
both  by  compression  of  the  larynx  and  by  edema  of  the 
laryngeal  entrance.    It  may  also  be  due  to  the  phleg- 


DYSPNCEA   AND    CYANOSIS  33 

monous  inflammation  of  the  neck  extending  along  the 
lamellae  of  the  cervical  fascia  to  the  thoracic  cavity, 
which  also  spreads  to  the  mediastinal  and  subpleural 
cellular  tissue  and  penetrates  even  through  the  inter- 
vertebral spaces  into  the  spinal  canal.  Dysphagia, 
interscapular  pains  radiating  anteriorly  toward  the 
sternum,  and  racking  pains  in  the  extremities,  may 
appear  as  concomitant  manifestations  of  the  dyspnoea. 

Constriction  of  the  laryngeal  lumen  may  also 
occur  through  blood  effusions  from  without  after  trau- 
mata and  especially  if  pointed  objects,  which  have  been 
carelessly  swallowed,  enter  the  air  tract.  This  may 
occur  in  the  unconscious  or  insane,  in  sufferers  from 
anesthesia  of  the  laryngeal  mucous  membrane,  also  in 
diphtheria,  syphilis,  tabes,  syringomyelia,  affections  of 
the  pneumogastric  nerve  and  bulbar  paralysis,  but 
never  according  to  my  experience  in  hysteria. 

The  extension  of  aphthae  into  the  larynx  very  rarely 
produces  dyspnoea,  and  much  more  rarely  still  the  im- 
migration of  ascarides  into  the  larynx. 

Dyspnoea,  cyanosis,  stridor  and  alteration  of  the 
voice,  the  latter  becoming  snuffling,  quivering  and 
aphonic  as  in  croup,  may  be  due  to  laryngeal  stenosis 
in  retropharyngeal  abscesses,  which  occur  for  instance 
in  an  acute  form  in  young  children  after  an  infectious 
pharyngitis  and  lymphadenitis,  in  diphtheria,  scarlet 
fever  and  erysipelas.  The  painful  dysphagia,  the  rigid 
position  of  the  head  and  neck  inclining  toward  the 
healthy  side,  the  swelling  of  the  palate,  and  frequently 
the  painful  edema  of  the  lateral  cervical  region,  should 


34         DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

warn  the  physician  to  examine  the  posterior  faucial 
wall  in  order  to  detect  any  fluctuating  prominence. 
With  the  opening  of  the  abscess,  all  these  ill-boding 
symptoms  disappear  instantly,  although  a  short  cessa- 
tion of  respiration  may  occur  immediately  after  the 
operation,  as  it  does  after  tracheotomy,  but  this  is  not 
attended  with  any  untoward  consequences. 

Retropharyngeal  abscesses  emanating  from  caries 
of  the  cervical  vertebrae  do  not,  as  a  rule,  exhibit  any 
such  disquieting  manifestations;  if  they  produce  signs 
of  laryngeal  stenosis,  the  cyanosis  is  less  marked  than 
the  anemia  attributable  to  the  primary  affection. 
Perilaryngeal  abscesses  which  are  frequently  unat- 
tended with  hyperemia,  edema  and  fluctuation,  may 
lead  to  grave  dyspnoea  and  even  to  death  from  syncope. 
Sometimes  they  develop  without  symptoms,  following 
a  retropharyngeal  abscess  or  after  repeated  intubations 
of  the  larynx. 

DISEASES    OF    THE   TRACHEA 

In  constriction  of  the  lumen  of  the  trachea  both 
dyspnoea  and  cyanosis  occur,  as  in  laryngeal  stenosis 
under  similar  conditions.  The  respiration  is  charac- 
terized by  whistling  rales  which  reach  their  climax 
during  inspiration,  and  the  difficulty  in  breathing  is 
inspiratory,  though  not  so  marked  as  in  laryngeal 
stenosis.  The  inspiratory  downward  movement  of  the 
larynx  does  not  occur  in  tracheal  stenosis,  nor  does 
the  backward  inclination  of  the  head  nor  the  changes 
in  the  voice,  which  are  observed  only  in  paralysis  of 


DYSPNCEA   AND   CYANOSIS  35' 

the  recurrent  laryngeal  nerve.  The  deviations  from 
the  ordinary  type  depend  upon  the  site  and  other 
conditions  of  the  stenosis;  in  scars  and  new  forma- 
tions, for  instance,  the  gravest  disturbances  in  breath- 
ing may  occur  alternately  in  inspiration  and  in 
expiration,  or  occasionally  include  both  phases  of  respi- 
ration. 

Acute  tracheal  stenosis  may  be  caused  by  esophageal 
swellings  pressing  the  posterior  wall  of  the  trachea 
against  the  anterior.  Salvolini  described  a  case  in 
which  this  swelling  was  made  up  of  33  ascarides, 
clustered  together  in  a  bundle. 

GOITRE 

In  goitre,  dyspnoea  may  be  occasioned  by  various 
causes.  Women  suffering  from  goitre  may,  through 
swelling  of  the  thyroid,  experience  considerable  dysp- 
ncea  during  menstruation,  which  disappears  with 
the  menses.  In  malignant  goitre  the  dyspnoea  may  be 
produced  not  only  by  compression  of  the  trachea,  but 
also  by  pressure  on  the  bronchi  and  metastases  in  the 
lungs.  In  goitre  and  in  Basedow's  disease  toxic  and 
cardiac  factors  play  a  role. 

The  mobile  goitre  is  an  interesting  phenomenon.  It 
is  a  very  freely  movable  thyroid,  parts  of  which — 
though  they  are  usually  situated  at  the  normal  place 
in  the  region  of  the  first  tracheal  ring — ^are  aspirated 
sometimes  behind  the  sternum,  at  times  behind  the 
clavicle  into  the  right  or  left  mediastinum,  and  there 
produce  attacks  of  asphyxia  and  disturbances  of 
circulation  from  pressure  upon  the  trachea  and  the 


36        DISORDERS  OF  RESPIRATION  AND   CIRCULATION 

large  vessels.  In  some  cases  there  exists  abnormal 
mobility  of  both  trachea  and  larynx  from  above  down- 
ward. This  wandering  goitre  is  differentiated  by 
Wolfler  from  goUre  plongeant,  which,  situated  in  the 
retrosternal  or  retroclavicular  region,  is  drawn  down 
by  inspiration  in  consequence  of  its  own  mobility,  and 
reappears  at  expiration.  These  endothoracic  goitres 
may  cause  the  greatest  distress,  and  in  certain  move- 
ments of  the  head,  for  instance  to  the  front  or  back, 
may  lead  to  sudden  attacks  of  asphyxia,  accom- 
panied by  cyanosis.  An  endothoracic  goitre  is  rec- 
ognized by  the  immobility  of  the  larynx  during 
deglutition  and  the  participation  of  a  palpable  swelling 
in  the  upper  mediastinum  in  lateral  movements  of  the 
thyroid. 

It  is  worth  mentioning  that  by  treatment  with  thyro- 
iodin  a  goitre  may  be  made  smaller  and  mobile.  If 
it  is  displaced  behind  the  sternum,  due  to  the  contrac- 
tions of  the  stemocleido-mastoid,  there  may  be  tension 
on  the  pneumogastric  nerve,  followed  by  cardiac  ar- 
rhythmia and  even  dilatation.  Thus  it  may  happen, 
as  seen  in  one  of  my  own  cases,  that  the  administration 
of  thyro-iodin  improves  the  manifestations  of  tracheal 
stenosis,  but  that  in  consequence  of  the  reduction  and 
migration  of  the  goitre  which  this  treatment  produces, 
grave  manifestations  may  make  themselves  manifest 
on  the  part  of  the  pneumogastric  nerve,  and  the  stenotic 
dyspnoea  may  give  way  to  a  cardiac  one.  In  the  case 
referred  to,  operative  removal  of  the  goitre  did  away 
with  the  tension  on  the  pneumogastric  nerve,  and  after 


DYSPNCEA   AND   CYANOSIS  37 

the  operation  all  cardiac  symptoms,  arrhythmia,  dysp- 
noea and  cyanosis  disappeared,  at  least  for  a  few 
months. 

AFFECTIONS    OF    THE    BRONCHI 

In  bronchial  stenosis,  inspiratory  dyspnoea  occurs 
with  rarefication  of  the  air,  but  only  in  the  section  of 
the  thorax  affected;  hence  unilateral  retraction  of  the 
corresponding  half  of  the  chest  with  inspiratory  retrac- 
tion and  immobility  of  the  edges  of  the  lungs.  In 
stenosis  of  high  degree  there  may  be  immobility  of 
the  intercostal  spaces,  the  supraclavicular  region  and 
the  epigastrium.  Auscultation  reveals  diminished 
breath  sounds  or  loud  dry  rales  on  the  side  of  the 
stenosis.  The  cause  of  the  constriction  is  most  fre- 
quently pressure  from  without  by  tumors  of  the  thy- 
roid, thymus,  esophagus,  of  the  mediastinum,  the 
lymphatic  glands  and  the  lung,  from  cold  abscesses 
due  to  spinal  caries,  dermoid  cysts,  also  from  aortic 
aneurisms  and  large  pericardial  exudates.  It  may, 
however,  be  caused  by  inflammatory,  ulcerative,  cicatri- 
cial and  carcinomatous  constrictions  of  the  bronchial 
wall  itself.  In  one  case  there  was  a  gummatous  in- 
filtration at  the  point  where  the  left  bronchus  branches 
off,  accompanied  by  considerable  asthmatic  trouble 
which  yielded  to  an  energetic  inunction  cure. 

In  cases  where  foreign  bodies  are  the  cause  of  the 
stenosis,  an  important  diagnostic  sign  is  furnished  by 
change  in  the  stenotic  manifestations  and  dyspnoea  with 
change  in  position  of  the  foreign  body.  Substances 
taken  into  the  larynx  usually  produce   most  violent 


38        DISORDERS  OF  RESPIRATION   AND   CIRCULATION 

manifestations  at  first,  while  at  subsequent  periods 
there  may  be  not  only  an  abatement  of  the  complaints, 
but  even  a  remarkable  tolerance  on  the  part  of  the 
mucous  membrane.  If  the  foreign  body  is  situated 
near  the  posterior  laryngeal  wall,  edema  of  the  ary- 
tenoid region  will  rapidly  occur  with  hoarseness, 
dysphagia,  irritant  cough,  bloody  expectoration  and 
dyspnoea,  while  foreign  bodies  in  the  recessus  pyri- 
formis  usually  cause  less  distress.  In  addition  to 
the  primary  changes  induced  by  foreign  bodies  in  the 
larynx,  there  may  be  subsequent  disturbances  such  as 
local  inflammations,  edema,  decubitus,  abscesses,  peri- 
chondritis and  inflammations,  which  may  extend  to 
the  mediastinum. 

If  a  foreign  body  is  expelled  from  the  larynx  into 
the  trachea,  it  may  be  forced  back,  and  after  a  possible 
repetition  of  this  excursion  finally  arrive  in  the 
bronchus.  During  this  migration  the  symptoms,  of 
course,  vary  with  each  change  of  position,  violent 
paroxysms  of  coughing  and  suffocation  alternating 
with  periods  of  relative  wellbeing.  In  these  cases  the 
dyspnoeic  attack  shows  the  expiratory  type,  and  the 
spastic  cough  may  assume  a  pertussis-like  character. 
Foreign  bodies,  however,  may  remain  in  the  trachea 
practically  without  causing  distress  or  symptoms. 

An  irritating  cough  with  purulent  and  sometimes 
bloody  expectoration,  which  narcotics  are  unable  to 
suppress,  and  frequently  followed  by  signs  of  circum- 
scribed pulmonary  gangrene  and  pleuritis,  is  an  im- 
portant sign  in  the  diagnosis  of  foreign  bodies  which 


DYSPNCEA   AND    CYANOSIS  39 

have  penetrated  into  the  small  bronchi.  This  is  valu- 
able in  cases  where  the  anamnesis  does  not  furnish  a 
sufficient  clue,  as  is  frequently  the  case  with  children. 
I  have  myself  observed  a  case  where  the  sputum  was 
even  fetid  and  a  circumscribed  pulmonary  focus  with 
pleuritis  was  demonstrable.  After  the  patient  had 
expectorated  a  small  piece  of  chicken  bone  of  whose 
aspiration  he  had  had  no  knowledge  whatever,  all 
pathological  manifestations  subsided. 

A  cardiac  cause  of  dyspnoea  may  also  be  present 
in  affections  of  the  respiratory  system.  Grave  dis- 
turbances of  respiration  with  cyanosis  are  met  with 
in  many  forms  of  bronchitis,  especially  in  the  acute, 
grave,  febrile  bronchitis  of  children,  also  in  senile 
bronchiolitis,  where  the  grave  dyspnoeic  paroxysms 
may  also  be  caused  by  acute  dilatation  of  the  heart,  a 
fact  which  should  be  borne  in  mind  for  the  therapy. 

There  may,  however,  be  dyspnoea  in  bronchitis,  al- 
though both  ventricles  functionate  perfectly,  and  other 
factors  must  then  be  held  responsible.  Thus,  there  is 
considerable  dyspnoea,  while  cyanosis  is  wholly  absent 
or  barely  indicated,  in  those  forms  of  bronchitis, 
with  severe  onset,  similar  to  catarrhal  forms  of  bron- 
chial asthma,  and  characterized  by  a  few  fine  rales. 
They  cause  the  most  alarming  symptoms  especially  in 
children,  but  after  a  short  course,  terminate  favor- 
ably. In  these  cases  the  physician  may  easily  be 
misled  into  the  diagnosis  of  capillary  bronchitis,  whose 
prognosis  is  very  different.  A  knowledge  of  the  fact 
that  the  patient  has  already  suffered   from  similar 


40         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

attacks  before  or  that  the  parents  were  asthmatic  may 
help  to  make  the  correct  diagnosis. 

BRONCHIAL    ASTHMA 

The  pathological  picture  of  bronchial  asthma  is 
composed  of  neurotic,  catarrhal  and  pulmonary  factors, 
one  or  another  predominating  in  each  case.  The 
asthmatic  nature  of  the  dyspnoea  is  seen  in  the  rapid 
onset  of  the  attack  and  the  exacerbation  of  the  difficulty 
in  breathing  to  an  alarming  extent,  almost  to  suffoca- 
tion. But  the  storm  abates  very  soon  and  the  patient 
returns  to  his  former  normal  condition.  A  paroxysm 
of  this  kind  is  recognized  either  by  the  unexpectedness 
of  the  attack,  or  by  prodromal  nerA^ous  symptoms,  as 
constriction  of  the  chest,  unpleasant  sensations  in  the 
intestine,  at  times  nasal  manifestations  such  as  sneezing 
or  coryza.  This  is  followed  by  rapidly  developing 
dyspnoea,  accompanied  by  sibilant  rales  in  which  expi- 
ration especially  is  aggravated  and  prolonged,  and 
accomplished  only  with  the  aid  of  all  the  expiratory 
muscles,  especially  the  abdominal.  Expectoration  is 
scanty  and  contains  large  quantities  of  eosinophile  cells, 
Curschmann's  spirals  and  Charcot's  crystals.  There  is 
distention  of  the  lungs.  The  expiratory  character  of 
the  breathing  with  protraction  of  the  expiratory  phase 
at  the  expense  of  inspiration,  and  frequently — though 
not  always — retardation  of  respiration,  places  its 
stamp  upon  this  paroxysmal  neurosis.  Cases  in  which 
inspiration  is  likewise  prolonged  and  the  frequency 
of  respiration  strikingly  increased,  rouse  the  suspicion 


DYSPNOEA   AND   CYANOSIS  4I 

of  simultaneous  complication  of  the  larger  bronchi, 
of  the  parenchyma  of  the  lung-s  or  of  the  heart. 

In  simple,  uncomplicated  asthma  there  is  no  cya- 
nosis, the  pulse  is  of  normal  tension  and  frequency 
and  only  moderately  accelerated.  As  the  affection 
proceeds,  the  transitory  pulmonary  distention  develops 
into  a  permanent  emphysema,  and  in  asthmatic  par- 
oxysms both  cyanosis  and  increased  frequency  of 
respiration  during  the  attack  are  often  observed. 
Sometimes  blood  is  mixed  with  the  sputum,  and  these 
hemorrhages  are  the  source  of  the  hemosiderin  pig- 
ment of  the  alveolar  epithelia  and  leucocytes.  It  fol- 
lows, therefore,  that  the  hemosiderin  cells,  commonly 
called  heart  failure  cells,  are  by  no  means  the  exclusive 
diagnostic  criterion  of  cardiac  asthma.  Similarly,  the 
presence  of  Curschmann's  spirals  and  of  eosinophile 
cells  alone  is  not  sufficient  to  decide  the  neuro-asthmatic 
nature  of  the  affection,  as  there  are  also  cases  of  car- 
diac asthma  with  spirals  and  eosinophile  cells. 

A  forty-six-year-old  patient  for  three  years  prior  to 
his  admission  into  the  clinic  suffered  from  asthmatic 
paroxyms  and  cough,  especially  when  climbing 
mountains  and  doing  hard  work.  The  dyspnoeic 
paroxysms  were  accompanied  by  oppression  of  the 
chest,  rales  and  profuse  perspiration,  lasting  about  a 
quarter  of  an  hour,  and  recurring  more  frequently  at 
night.  Later  there  was  edema  of  the  legs  and  dis- 
tention of  the  abdomen.  Auscultation  during  the  at- 
tack showed  diminished  respiration  with  rales  and 
prolonged  expiration.     Besides,  there  were  the  phys- 


42         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

ical  signs  of  insufficiency  of  the  aortic  valves.  Blood 
pressure  115.  Upon  the  administration  of  digitalis 
and  especially  theocin  there  was  abundant  diuresis  and 
considerable  improvement  in  the  general  condition. 
To  all  appearances  this  was  a  case  of  cardiac  asthma. 
Sputum  during  the  attacks  was  rather  plentiful,  muco- 
serous,  with  muco-purulent  flakes^  some  of  which  were 
very  tenacious.  These  portions  showed  under  the  mi- 
croscope dense  mucous  filaments  arranged  in  spirals, 
and  among  them  typical  Curschmann's  spirals  with 
central  filament.  Aside  from  numerous  pus  corpus- 
cles there  were  a  few  scattered  eosinophile  cells  and, 
likewise  a  great  many  heart  failure  cells  with  partly 
diffuse,  partly  clumpy,  brownish-yellow  pigment.  In 
a  few  fields  there  were  also  numerous  erythrocytes  ar- 
ranged in  long  rows  corresponding  to  the  mucous 
threads.  From  the  clinical  point  of  view  we  had  only 
a  cardiac  asthma  to  deal  with,  while  the  microscopic 
finding  of  the  sputum  in  addition  to  the  heart  failure 
cells  and  erythrocytes  showed  additional  elements 
which  belong  to  bronchial  asthma,  as  eosinophile  cells 
and  Curschmann's  spirals.  Paroxysmal  attacks  of 
dyspnoea  which  are  exceedingly  similar  to  bronchial 
asthma,  with  sibilant  rales  and  prolonged  expiration 
also  occur  in  chronic  influenza,  in  which,  aside  from 
eosinophile  cells,  there  are  microscopically  and  cultur- 
ally demonstrable  small  numbers  of  Pfeiffer's  influenza 
bacillus.  Cases  of  this  kind  have  been  observed  re- 
peatedly at  our  clinic;  Lord  has  mentioned  such  cases 
and  Ortner  described  several  of  them.     Sputum  prep- 


DYSPNCEA   AND   CYANOSIS  43 

arations,  stained  merely  with  fuchsin,  revealed  the 
presence  of  the  small  cocco-bacillus  and  also  an  abun- 
dant sputum  flora^  while  asthmatic  sputum  is  poor  in 
bacteria.  Patients  recovering-  from  influenzal  infec- 
tions may  likewise  present  the  symptom-complex  of 
asthma,  although  they  had  never  suffered  from  this 
affection.  This  provocatory  effect  of  influenza  may 
show  itself  in  the  evanescent  stage  of  the  primary  af- 
fection and  then  herpes  facialis  may  develop. 

A  female  nurse,  twenty-eight  years  of  age,  was 
received  at  our  clinic  suffering  from  asthma  with  pre- 
menstrual exacerbation  of  the  attack,  during  which  the 
blood  pressure  was  reduced.  The  sputum  contained 
eosinophile  cells,  no  Charcot's  crystals,  and  was  poor 
in  bacteria.  A  month  prior  to  the  occurrence  of  these 
attacks  she  had  recovered  from  influenza.  These 
attacks  of  asthma  following  after  influenza  suggest  a 
toxic-infectious  factor,  exercising  an  effect  upon  the 
pulmonary  terminals  of  the  pneumogastric  nerve,  the 
elimination  of  which  may  perhaps  become  possible  by 
suitable  antisera.  Boucheron  reports  cases  of  asthma, 
which  are  said  to  have  been  cured  by  antistreptococcus 
serum. 

The  clinical  picture  of  bronchial  asthma,  the  se- 
quence of  symptoms,  the  recurrence  of  paroxysms  and 
the  sputum  findings,  offer  sufficient  material  for  dif- 
ferentiation from  those  forms  of  a  typical  angina 
pectoris,  in  which  there  is  also  expiratory  dyspnoea. 
At  the  same  time  there  are  many  cases  of  bronchial 
asthma  which  may  offer  diagnostic  difficulties  if  they 


44        DISORDERS  OF  RESPIRATION   AND   CIRCULATION 

occur  in  youthful  cardiac  patients.  This  is  pre-emi- 
nently the  case  in  affections  of  the  aorta  which  develop 
on  a  syphilitic  basis.  An  exact  observation  of  the 
attacks,  the  anamnesis,  the  general  impression  of  the 
patient,  and  the  success  of  the  selected  therapy  are 
alone  decisive. 

Paroxysmal  attacks  of  dyspnoea  in  aneurism  of 
the  aorta,  especially  in  youthful  patients,  may  likewise 
give  rise  to  considerable  perplexity,  particularly  when 
the  physician  adheres  to  the  asthmatic  symptom-com- 
plex or  to  a  preconceived  notion,  and  at  the  same  time 
neglects  an  X-ray  examination.  The  pronounced 
character  of  the  expiratory  dyspnoea  distinguishes 
bronchial  from  cardiac  asthma  and  aneurismal  asthma, 
and  also  from  laryngospasm  and  all  conditions  of  in- 
spiratory dyspnoea,  as  spasm  of  the  diaphragm  and 
tetany,  in  which  spastically  prolonged  inspiration 
passes  by  a  sudden  transition  into  unobstructed  ex- 
piration. In  many  forms  of  bronchial  asthma  there 
is  inspiratory  bulging  of  the  epigastrium  and  expira- 
tory flattening  of  the  same,  which  is  diagnostically 
valuable  in  contradistinction  to  the  tonic  spasm  of  the 
diaphragm. 

Bronchial  asthma  thus  presents  a  complete  patho- 
logical picture,  and  in  most  cases  there  is  no  particular 
difficulty  in  the  diagnosis,  but  cases  occur  in  which 
anatomical  lesions  of  the  pneumogastric  nerve  develop 
quite  a  similar  appearance,  so  that  one  might  speak  of 
a  pneumogastric  asthma.  In  explaining  the  mechan- 
ism of  essential  bronchial  asthma  an  exciting  process 


DYSPNCEA   AND   CYANOSIS  45 

must  be  assumed  to  exist.  This  lies  in  the  tract  of 
the  pneumogastric,  exerts  its  effect  on  its  respiratory, 
vasomotor  fibers  and  leads  to  spasm  of  the  bronchial 
muscles.  The  catarrhal  manifestations  are  to  be  looked 
upon  as  a  sequence  of  the  vaso-dilatation  and  hy- 
peremia of  the  bronchial  mucous  membrane,  a  second- 
ary factor,  which  is  superadded  to  the  spastic  element. 

Such  cases  as  a  typical  bronchial  asthma  accom- 
panying a  carcinoma  of  the  lungs,  observed  by  A. 
Schmidt,  and  paroxysms  resembling  asthma  due  to 
irritation  of  the  pneumogastric  from  pressure  of 
enlarged  glands  in  measles,  whooping  cough  and 
tuberculosis,  observed  by  Biermer,  illustrate  the  occa- 
sional difficulties  of  diagnosis  and  warn  us  not  to  omit 
the  X-ray  examination  in  cases  which  are  not  abso- 
lutely clear. 

The  importance  of  vasomotor  changes  in  asthma  is 
especially  illustrated  by  cases  in  which  other  vasomotor 
equivalents,  such  as  dermographism,  perspiration, 
tachycardia,  hemicrania  and  angioneurotic  edema, 
occur  simultaneously  or  alternately  with  asthmatic 
paroxysms.  In  these  cases  a  rapid,  angioneurotic 
swelling  of  the  mucous  membrane,  due  to  a  dilatation 
of  the  bronchial  vessels,  may  lead  to  a  diminution  of 
the  lumen  of  the  bronchioles  and  in  this  way  the  asth- 
matic paroxysms  without  spasm  of  the  bronchioles  are 
explainable.  This  angioneurotic  hyperemia  has  al- 
ready been  obsei-ved  by  Stoerck  and  Pieniazek  in  a 
tracheoscopic  examination  of  the  lower  part  of  the 
trachea  and  at  the  entrance  into  the  bronchi  and  su^- 


46        DISORDERS   OF  RESPIRATION   AND  CIRCULATION 

gests  that  the  hyperemia  may  also  spread  to  the  bron- 
chial ramifications.  In  these  vasomotor  forms  o£ 
asthma,  amylnitrit,  will — according  to  Solis-Cohen — 
aggravate  the  intensity  of  the  paroxyms;  adrenal 
preparations,  on  the  other  hand,  administered  internally 
for  a  long  period,  are  said  to  cure  the  attacks,  while 
the  same  medication  is  without  benefit  in  ordinary 
bronchial  asthma. 

Thus  it  will  be  seen  that  aside  from  the  mixed  forms 
of  bronchial  asthma,  where  all  the  components — neu- 
rotic, bronchitic  and  pulmonary,  act  together,  there 
are  also  cases  in  which  the  spastic  or  angioneurotic 
form  assumes  special  importance  in  the  pathological 
picture.  These  clinical  observations  are  not  contra- 
dicted by  the  results  of  animal  experiments,  which 
have  demonstrated  on  the  one  hand  both  vaso-con- 
strictors  and  vaso-dilators  in  the  pneumogastric,  and 
teach  on  the  other  hand,  according  to  Sihle's  experi- 
ments, that  peripheral  irritation  of  the  pneumogastric 
nerve  can  produce  a  bronchostenosis  from  muscular 
spasm.  These  findings  should  be  duly  considered 
in  the  selection  of  the  therapy,  which  in  one  case  con- 
sists of  vagus  poisons,  atropin,  datura,  hyoscyamus, 
and  in  other  cases  attacks  the  vasodilator  element 
(adrenalin).  At  the  same  time  the  etiological  factor 
should  be  kept  in  mind — for  instance  in  urticaria — 
by  avoiding  noxious  causes  or  removing  possible  meta- 
bolic anomalies  as  factors  favoring  asthma  (uric  acid 
diathesis) . 

The  importance  of  predisposition  is  especially  il- 


DYSPNCEA   AND   CYANOSIS  47 

lustrated  by  cases  in  which  nervous  asthma,  like  hay- 
asthma,  occurs  only  during  pregnancy  and  so  becomes 
a  sign  of  pregnancy.  Whether  in  these  cases  asthma 
is  caused  by  irritation  of  the  pneumogastric  or  by  in- 
toxication is  an  unsettled  question.  The  prognosis 
in  these  cases  is  serious  for  both  mother  and  child  and 
may  be  an  indication  for  an  artificial  premature  de- 
livery. 

PERTUSSIS 

Paroxysmal  dyspnoea,  coupled  with  cyanosis,  occurs 
in  the  spasmodic  coughing  of  pertussis,  but  in  contra- 
distinction to  asthma  there  is  a  protracted  sibilant  in- 
spiration followed  by  a  series  of  short  expiratory  puffs. 
Increased  pressure  within  the  thorax  produces  an  en- 
gorgement of  the  venae  cavae,  and  the  appearance  of 
dyspnoea  and  cyanosis  in  uncomplicated  whooping 
cough  is  associated  only  with  the  attacks  of  coughing. 
In  complications,  however,  as  marked  dilation  of  the 
lungs,  interlobular  emphysema,  pneumothorax,  or  less 
frequently  edema  of  the  glottis,  dyspnoea  and  cyanosis 
will,  as  a  matter  of  course,  outlast  the  attacks.  Should 
a  febrile  affection,  an  acute  exanthema,  supervene,  the 
paroxysms  of  whooping  cough  grow  less  in  intensity 
and  frequency,  and  together  with  them  the  dyspnoea 
and  cyanosis. 

Permanent  cyanosis  in  pertussis  with  coincident  les- 
sening in  the  attacks  of  coughing  is,  as  it  Is  after 
measles,  an  important  diagnostic  sign  of  bronchopneu- 
monia, edema  of  the  bronchial  glands,  and  later  tuber- 
culosis of  the  glands.     In  these  latter  cases,  dyspnoea 


48         DISORDERS   OF   RESPIRATION   AND  CIRCULATION 

and  cyanosis  occur  from  compression  of  the  bronchi, 
veins  and  nerv'-es,  and  it  is  just  in  cases  where  the  re- 
current laryngeal  nerve  reacts  against  the  pressure  by 
irritative  phenomena,  that  a  wrong  diagnosis  of  re- 
lapsed pertussis  may  be  made  owing  to  the  pertussis- 
like paroxysms  thereby  produced.  For  this  reason 
dyspnoea  and  cyanosis  with  swelling  of  the  cer\ncal 
veins  outlasting  the  paroxysms  demand  a  careful  ex- 
amination of  the  larynx  and  the  thoracic  organs,  in- 
cluding an  X-ray  examination. 

FIBRINOUS   AND    CAPILLARY   BRONCHITIS 

Considerable  difficulty  in  breathing,  with  cyanosis, 
fever,  frothy  and  sometimes  bloody  expectoration,  is 
obsen^ed  in  acute  fibrinous  bronchitis.  In  chronic  fe- 
brile, fibrinous  bronchitis,  cyanosis  with  violent  par- 
oxysms of  coughing  and  at  times  also  hemoptysis, 
previous  to  the  expectoration  of  the  plugs,  are  char- 
acteristic signs  and  have  a  diagnostic  importance  in 
cases  where  simple,  subacute,  bronchial  catarrh  under- 
goes a  transition  into  fibrinous  bronchitis. 

Chronic,  fibrinous  bronchitis  at  times  displays  an 
intermittent  course,  reminding  one  in  the  beginning 
of  an  attack  of  bronchial  asthma.  I  observed  a  case 
in  which,  preceding  the  expectoration  of  the  character- 
istic clots,  the  tenacious  sputum  contained  large  num- 
ber of  eosinophile  cells  and  Charcot's  crystals.  In 
the  t}'pical  cases  of  chronic,  fibrinous  bronchitis,  lead- 
ing to  the  constriction  of  the  bronchial  lumen,  the 
mechanical  factor  and  therefore  inspiratory  dyspnoea 


DYSPNCEA   AND   CYANOSIS  49 

prevails,  while  in  bronchial  asthma  the  neurotic  factor^ 
and  with  it  expiratory  dyspnoea,  predominates. 

The  plugs  in  symptomatic,  pseudofibrinous  bron- 
chitis, which  occurs  in  ulcerative  processes  and  espe- 
cially in  syphilis  of  the  trachea  and  bronchi,  consist  of 
desquamated  layers  of  the  ulcers,  whereas  the  bron- 
chial clots  of  true  fibrinous  bronchitis  represent  secre- 
tory products  from  a  relatively  unimpaired  mucous 
membrane.  Membranous  masses  in  the  bronchi  may 
also  be  developed  by  tubercular  bronchial  ulcers  and 
may  lead  to  grave  dyspncea.  Fibrinous  bronchitis 
occurs  in  acute  inflammation  of  the  lungs,  due  to  the 
extension  of  the  alveolar  affection  to  the  bronchi,  and 
in  these  cases  dyspnoea  is  one  of  the  most  prominent 
signs.  In  other  cases,  fibrinous  bronchitis  follows  in 
the  wake  of  laryngeal  and  tracheal  croup.  A  rare  case 
of  membranous  bronchitis  was  observed  by  Renon  in 
a  thirty-nine-year-old  woman  whose  occupation  was 
to  sort  grain  in  a  moist  room.  She  expectorated  whit- 
ish green,  non-arborescent  membranes  which  consisted 
exclusively  of  aspergillus  mycelia  and  spores. 

In  cases  where  ordinary  bronchitis  extends  consider- 
ably there  may  be  early  and  great  difficulty  in  breath- 
ing with  cyanosis,  so  that  from  a  clinical  standpoint 
the  designation  of  suffocative  bronchitis  is  justified.  In 
capillary  bronchitis  especially,  the  continuous  and  pro- 
gressive dyspnoea  with  markedly  increased  frequency 
of  respiration  may  assume  a  suffocative  character  and 
be  fatal  from  asphyxia  by  occlusion  of  the  smallest 
bronchi,  due  to  edema  of  the  mucous  membranes  or 


50         DISOEDERS  OF  RESPIRATION  AND  CIRCULATION 

to  the  secretion.  At  the  same  time  there  may  also  be 
cardiac  disorders  in  acute  bronchitis,  particularly  in 
influenzal  bronchitis,  probably  in  consequence  of  the 
toxic  effect  of  the  infectious  causative  factors.  These 
forms  of  bronchitis  may  recur  in  circumscribed  foci, 
accompanied  by  a  great  increase  in  dyspnoea  and 
cyanosis,  but  according  to  Fr,  Miiller  they  do  not 
directly  imply  danger  to  life.  The  results  are  different, 
if  the  dyspnoea  continues  progressive,  as  in  bronchio- 
litis fibrinosa  obliterans,  which  leads  to  occlusion  of 
the  finest  bronchioles  by  connective  tissue,  and  through 
impeding  respiration  causes  death  by  suffocation  in  the 
shortest  possible  time.  According  to  Fraenkel  the 
possibility  of  bronchiolitis  obliterans  should  be  borne 
in  mind  when  these  grave  symptoms  develop  in  a  pre- 
viously healthy  individual  whose  organs  of  respiration 
have  been  exposed  to  external,  irritating  influences,  as 
steam  or  dust. 

In  the  chronic  forms  of  bronchitis  and  in  long-con- 
tinued illnesses,  dyspnoea  develops  in  consequence  of 
fatty  degeneration  of  the  right  ventricle  of  the  heart 
even  where  the  secondary  emphysema  is  of  slight 
extent. 

If  in  bronchitis  there  is  high  fever  with  cyanosis, 
dyspnoea  and  great  frequency  of  respiration,  it  consti- 
tutes diagnostically  and  prognostically  an  important 
symptom-complex  which  may  point  to  the  complication 
of  simple  bronchitis  with  broncho-pneumonia. 

Focal  bronchitis  with  rales  occurs  in  areas  where 
the  visceral  pleura  is  adherent  to  the  costal  pleura, 


DYSPNCEA   AND   CYANOSIS  51 

producing  atelectasis  and  broncho-pneumonic  foci. 
Sometimes  acute  infectious  bronchitis  may  be  com- 
plicated by  the  formation  of  multiple  bronchiectases, 
which  add  to  the  pathological  picture  an  entirely  new 
symptom — the  intermittent  expectoration  of  large 
quantities  of  muco-purulent  sputum  in  paroxysms  of 
suffocation. 

In  chronic  bronchiectasis,  dyspnoea  and  cyanosis 
mostly  depend  upon  the  size  of  the  cavities  which  may, 
if  complicated  with  heart  disease  or  emphysema,  at- 
tain a  great  size. 

Dyspnoea  with  accelerated  superficial  respiration  and 
inspiratory  retractions  of  the  thorax  also  occurs  in  ex- 
tensive pulmonary  atelectasis.  The  degree  of  dysp- 
noea and  cyanosis  as  well  as  the  other  signs  of  the 
pathological  picture  depend  upon  both  the  original 
cause  of  the  atelectasis  and  the  concomitant  complica- 
tions. 

PNEUMONIA 

Dyspnoea  in  acute  pneumonia  is  of  frequent  occur- 
rence and  is  explained  by  the  diminution  of  the  res- 
piratory surface  with  lessened  inspiration  in  conse- 
quence of  reduced  power  of  muscular  contraction  and 
of  pleuritic  pains.  Dyspnoea,  however,  does  not  al- 
ways exist  in  direct  proportion  to  the  pathological 
changes  in  the  lungs.  It  may  be  very  considerable  in 
spite  of  the  slight  extent  of  the  pneumonic  affec- 
tion, and  again  it  may  be  absent  although  an  entire 
lung  is  infiltrated.  At  the  time  of  the  crisis,  all 
of  the  symptoms  may  recede,  although  the  physical 


52         DISORDERS  OF   RESPIRATION   AND  CIRCULATION 

findings  of  the  lungs  disclose  no  change  whatever.  It 
may  be  assumed  that  dyspnoea  in  pneumonia  depends 
not  only  on  the  mechanical  factor,  but  also  on  the  toxic 
influence  of  the  pathological  causative  factors  upon  the 
center  of  respiration  and  also  on  the  degree  of  sus- 
ceptibility of  the  latter.  Generally  speaking,  it  may 
be  said  that  dyspnoea  out  of  proportion  to  the  extent 
of  the  local  changes,  especially  if  the  respirations  are 
very  frequent  and  irregular  in  the  absence  of  local 
causes,  such  as  pain  or  hysteria,  justifies  an  unfavor- 
able prognosis. 

In  simple,  uncomplicated  pneumonia  cyanosis  is  a 
late  symptom  and  proportionate  to  the  progressive 
change  in  the  area  of  respiration  and  is  most  pro- 
nounced, therefore,  in  bilateral  pneumonia.  In  most 
cases,  early  cyanosis  associated  with  dyspnoea  means 
involvement  of  the  heart,  such  as  frequently  occurs  in 
grave  senile  pneumonia  and  in  alcoholics.  In  these 
cases  cyanosis  may  occur  with  accelerated  respiration 
and  slightly  irritating  cough,  but  without  any  sub- 
jective dyspnoea. 

Dyspnoea  and  cyanosis  may  also  be  dependent  upon 
the  nature  of  the  pathological  cause,  even  if  the  extent 
of  the  pneumonic  condition  be  slight,  as  in  influenzal 
pneumonia,  streptococcal  pneumonia,  but  particularly 
in  the  pneumonia  of  diphtheria,  the  plague,  and  gland- 
ers, in  which  not  only  the  toxic  influence  upon  the 
respiratory  center,  but  also  the  direct  injury  to  the 
heart  plays  a  role.  A  peculiar  combination  of  cyanosis 
and  icterus  is  observable  in  septic  pneumonia,  in  which 


DYSPNCEA   AND   CYANOSIS  53 

high  temperature,  loss  of  consciousness,  delirium,  coma 
and  accelerated  respiration  should  be  regarded  as  a 
frequent  premortal  symptom-complex. 

Deep  cyanosis  may  also  occur  in  pneumonia  com- 
plicated with  thyroiditis,  mediastinitis,  endocarditis, 
pericarditis,  also  with  malaria  with  rapid  elevation 
of  temperature  and  in  secondary  pneumonia  in  conse- 
quence of  carbonmonoxid  poisoning,  in  pneumonia 
resulting  from  foreign  bodies,  including  deglutition 
pneumonia  as  occurs  in  persons  rescued  from  drown- 
ing. Early  dyspnoea  and  cyanosis  with  abnormally 
increased  frequency  of  pulse  and  not  excessive  tem- 
perature has  been  observed  in  the  so-called  asthenic 
forms  of  pneumonia,  and  also  in  those  cases  which  de- 
velop into  pulmonary  gangrene.  In  all  of  these,  there 
are  other  symptoms  to  indicate  the  malignant  type  of 
the  disease,  as  enlargement  of  the  spleen  and  liver, 
icterus,  meteorism,  nephritic  manifestations,  cya- 
nosis, prostration:  signs  of  grave  general  infection  or 
intoxication.  For  this  reason  it  should  always  be  con- 
sidered a  prognostically  unfavorable  sign,  if  there  is 
early  cyanosis  in  pneumonia  and  progressively  increas- 
ing frequency  of  pulse  without  corresponding  eleva- 
tion of  temperature,  particularly  if  the  pneumonic 
affection  is  only  of  slight  extent. 

Dyspncea  and  cyanosis  attain  a  high  degree 
when  pneumonia  attacks  individuals  whose  cardiac 
muscle  was  previously  degenerated,  as  in  pre-existing 
myocarditis,  or  in  obese  persons  with  dilatation  of 
the  right  ventricle.     In  these  cases  the  clinical  picture 


54         DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

will  also  disclose  other  signs  of  cardiac  inefficiency, 
such  as  abnormally  high  frequency  of  pulse,  weak 
heart  sounds,  arrhythmia  and  low  blood  pressure. 

Of  prognostic  importance  are  those  forms  of  pneu- 
monia which  complicate  a  pre-existing  mitral  stenosis, 
because  it  admits  of  the  erroneous  diagnosis  of  myo- 
carditis, if  the  valvular  lesion  is  not  betrayed  by  typ- 
ical signs  and  if  the  arrhythmia  with  a  small,  weak 
pulse  stands  in  the  foreground  of  the  symptoms.  In 
these  cases  marked  cyanosis  and  dyspnoea  may  undergo 
improvement  under  the  administration  of  digitalis. 

Dyspnoea  and  cyanosis  may  occasionally  appear  in 
pneumonia  just  before  the  crisis  in  consequence  of 
dilatation  of  the  right  ventricle,  if  there  occurs  a  back- 
ward engorgement  of  the  blood  to  the  right  heart 
from  extension  of  the  infiltration  and  if  there  are 
manifestations  of  edema  of  the  lung.  In  progressive 
dilatation  of  the  right  ventricle,  with  accentuation  of 
the  second  pulmonary  sound,  cyanosis  and  manifesta- 
tions of  commencing  edema  of  the  lungs,  bleeding 
may  be  indicated,  even  in  the  case  of  a  rapid  and  weak 
pulse. 

Not  infrequently  cyanosis  is  the  result  of  a  sudden 
reduction  of  the  temperature  by  antipyretics.  This 
is  a  defebrile  symptom  which  occurs  if  the  cardiac 
muscles  which  had  been  excited  by  high  temperature 
no  longer  experience  this  abnormal  stimulation.  In 
the  administration  of  antipyrin  and  similar  febrifuges 
cyanosis  may  be  especially  pronounced. 

Sudden  cyanosis  and  dyspnoea  with  fatal  collapse 
through  paralysis  of  the  heart,  thrombosis  of  the  pul- 


DYSPNCEA   AND   CYANOSIS  55 

monary  veins  and  edema  of  the  lungs,  may  follow 
pneumonia,  in  convalescent  patients  who  have  left  the 
bed  too  early. 

Intense  dyspnoea  with  slight  fever  occurs  in  the 
pneumonia  of  diabetics.  It  may  take  a  lightning 
course,  and  lead,  with  manifestations  of  cyanosis  and 
coma,  to  a  prematurely  fatal  termination. 

In  pregnant  women  pneumonia  is  a  dangerous  com- 
plication, because  both  dyspnoea  and  cyanosis  may  at- 
tain considerable  proportions,  and  the  overcharge  of 
the  blood  with  carbon  dioxid  means  a  menace  to  both 
mother  and  child.  Pneumonia  in  hysteria  may  be  ac- 
companied by  a  high  degree  of  dyspnoea  standing  in 
no  proportion  to  the  extent  of  the  pneumonic  affec- 
tion. This  form  of  pneumonia  gives  rise  to  anxiety, 
but  subsides  in  a  normal  crisis.  Pronounced  tachy- 
pnoea  has  an  unfavorable  prognosis,  if  it  continues 
throughout  a  disease  in  which  the  respirations  rise 
to  sixty,  seventy  or  ninety,  but  hysteria  is  an  excep- 
tion. The  other  hysterical  stigmata  and  the  absence  of 
pronounced  cyanosis,  may  in  some  cases  of  this  de- 
scription indicate  the  correct  prognosis.  In  neuras- 
thenics, however,  pneumonia  as  well  as  other  infectious 
diseases  take  under  certain  conditions  a  mild  course 
and  there  may  even  be  a  favorable  influence  noticeable 
upon  the  nervous  symptoms,  as,  for  instance,  in  asthma. 

HYPEREMIA   OF   THE   LUNGS 

Dyspnoea  and  cyanosis  may  also  occur  in  hyperemia 
of  the  lungs.  These  hyperemias  may,  especially  in 
the  case  of  old  people  after  prolonged  decubitus,  lead 
rapidly  or  by  repeated  attacks  to  death  by  suffocation. 


56         DISORDERS  OF  RESPIRATION   AND   CIRCULATION 

But  here  again  there  are  cases  where  the  grave  mani- 
festations, even  with  pronounced  unconsciousness,  re- 
cede, until  after  a  time  the  same  picture  repeats  itself. 
In  a  case  I  observed,  the  autopsy  disclosed  atrophy  of 
the  brain.  Cutting  of  the  pneumogastric  nerve  causes 
hyperemia  and  edema  of  the  lungs.  It  appears, 
therefore,  that  in  the  development  of  pulmonary  hy- 
peremia increasing  to  an  edema,  not  only  the  me- 
chanical factor  of  cardiac  weakness,  but  also  dis- 
turbances of  pulmonary  innervation  in  the  sense  of  a 
vaso-paralysis  may  play  a  role.  This  can  be  observed 
in  cases  where  hyperemia  of  the  lungs  in  hemiplegia 
develops  unilaterally,  on  the  side  opposite  to  that  of 
the  cerebral  lesion. 

Gall  stones  may  reflexly  lead  to  hyperemia  of  the 
lung,  particularly  in  the  right  lower  lobe,  and  subse- 
quently to  dyspnoea.  Where  there  are  also  chills  and 
fever,  the  picture  of  pneumonia  may  be  simulated. 
Hyperemia  after  trauma  of  the  chest  and  colds,  es- 
pecially in  alcoholics,  leads  not  infrequently  to  edema 
of  the  lungs. 

EDEMA    OF   THE   LUNGS 

Dyspnoea  and  cyanosis  are  frequently  terminal  signs 
in  edema  of  the  lungs,  especially  in  affections  of  the 
organs  of  respiration  and  circulation.  There  should 
be  kept  in  mind  embolism  of  the  pulmonary  artery, 
bronchitis,  pneumonia,  pleuritis,  pulmonary  tuberculo- 
sis, myocarditis  and  cardiac  insufficiency ;  further,  acute 
exanthemata,  typhoid  and  especially  typhus,  recurrent 
fever,  influenza,  acute  articular  rheumatism,  grave  ma- 


DYSPNCEA   AND   CYANOSIS  5/ 

laria ;  in  rare  cases  alcoholic  poisoning,  carbonmonoxid 
poisoning,  snake  bites,  frost  bite  and  sunstroke;  lastly 
cerebral  affections,  especially  concussion  of  the  brain. 
Of  particular  interest  is  the  edema  of  the  lungs  occur- 
ring in  infections  due  to  the  bacterium  coli  as  in  incar- 
cerated hernia  and  perityphlitis,  In  which  the  bacterium 
coli  is  demonstrable  in  the  sputum.  Mention  should 
also  be  made  of  the  edema  of  the  lungs  in  the  aer- 
onaut and  that  arising  ex  vacuo  with  albuminous  ex- 
pectoration, which  appears  chiefly  after  thoracentesis, 
especially  where  there  are  pericardial  adhesions.  One 
of  the  most  frequent  causes  of  acute  edema  of  the 
lungs  is  disease  of  the  kidneys,  and  sometimes  pneu- 
monia of  very  slight  extent  in  nephritic  subjects  may 
lead  to  a  rapidly  fatal  edema  of  the  lungs. 

PULMONARY  EMBOLI  AND  THROMBI 

The  degree  of  dyspnoea  and  of  cyanosis  in  emboli  of 
the  pulmonary  artery  depends  chiefly  on  the  lumen 
of  the  occluded  branch.  Embolus  of  the  main  branch 
or  trunk  of  the  pulmonary  artery  leads  with  violent 
manifestations  to  sudden  death  from  syncope  or  to 
the  protracted  agony  of  suffocation.  In  the  former 
case  there  is  a  marked  oppression  with  pallor,  in  the 
latter  dyspnoea  with  protrusion  of  the  bulbi,  dilata- 
tion of  the  pupils  and  frequently  convulsions. 

If  the  course  of  pulmonary  embolism  be  protracted, 
cyanosis  may  attain  a  high  degree  and  be  accompanied 
by  swelling  of  the  jugular  veins,  venous  pulsation,  and 
sometimes  by  distinct  pulsation  in  the  epigastrium  as  a 
consequence  of  the  stormy  contractions  of  the  dilated 


58         DISORDERS  OF  RESPIRATION   AND   CIRCULATION 

right  ventricle.  This  is  contrary  to  the  asphyctic  form 
of  angina  pectoris,  which,  if  protracted,  sometimes 
develops  cyanosis  and  dyspnoea,  but  the  cardiac  func- 
tion is,  as  a  rule,  abnormally  weak  and  increased  func- 
tion of  the  right  ventricle  has  been  observed  only  ex- 
ceptionally in  hypertrophic  conditions. 

In  emboli  of  the  medium  and  small  branches  of  the 
pulmonary  artery,  the  onset  of  which  is  not  infre- 
quently accompanied  by  chill,  the  sudden  dyspnoea 
and  cyanosis  may  lessen  after  a  short  time,  only  to 
repeat  itself  or,  after  repeated  recurrences  may  lead  to 
a  fatal  edema  of  the  lungs,  to  pneumonia,  and  at  times 
to  recover}^  The  course  of  such  a  pulmonary  embolus 
which  does  not  lead  to  pneumonia  and  attacks  an  in- 
dividual, not  suffering  from  fever,  is  afebrile.  It  is 
just  the  absence  of  fever  after  preceding  initial  chill 
with  pleurodynia  and  bloody  expectoration,  which  is 
valuable  for  differentiation  from  pneumonia. 

In  emboli  of  the  small  branches,  there  are  at  first 
fainting  attacks,  frequently  followed  by  the  formation 
of  a  hemorrhagic  infarct  with  hemoptysis,  but  without 
cyanosis,  while  multiple  emboli  sometimes  lead  to  per- 
sistent dyspnoea  and  cyanosis  without  any  stormy  on- 
set. Dyspnoea  in  pulmonary  embolus  is  occasioned 
partly  by  exclusion  of  the  corresponding  section  of  the 
lungs,  in  part  by  effusion  of  blood  into  the  bronchi, 
partly  by  reflex  irritation  of  the  pneumogastric  nerve 
terminal  in  the  lungs,  and,  therefore,  does  not  always 
correspond  to  the  size  of  the  pulmonary  focus.  In 
attacks,    however,    with    marked   pulmonary   hemor- 


DYSPNCEA   AND    CYANOSIS  59 

rhage,  dyspnoea  is  very  intense  and  predominates  over 
the  cyanosis. 

Emboli  of  the  smallest  branches  of  the  pulmonary 
artery  at  times  do  not  produce  any  material  symptoms 
and  do  not  always  lead  to  hemoptysis.  But  here,  also, 
there  may  be  dyspnoea  and  cyanosis  in  consequence  of 
secondary  pleural  effusions  and  disseminated  broncho- 
pneumonia. 

It  is  a  well  known  fact  that  emboli  of  the  pulmonary 
artery  may  occur  in  the  course  of  the  most  varied  path- 
ological conditions.  They  may  follow  injuries  to  the 
head  by  the  detachment  of  thrombic  masses  from  the 
diploic  veins,  in  ileo-cecal  and  umbilical  phlebitis,  in 
thrombosis  of  the  femoral  veins,  in  occlusion  of  the 
prostatic  veins  or  pelvic  veins,  the  latter  frequently 
occurring  in  the  puerperium,  in  tuberculosis,  carcinoma, 
chlorosis,  infectious  diseases  and  during  convalescence. 
They  may  also  be  produced  by  massaging  a  leg  having 
varicose  veins  and  by  careless  manipulation  of  the 
extremities  of  persons  suffering  from  phlegmasia  alba 
dolens. 

In  fractures  of  the  long  bones,  pulmonary  emboli 
occur  partly  by  the  detachment  of  venous  thrombi,  in 
part  by  marrow  invading  the  open  veins  of  the  bones. 
Fat  emboli  may  also  occur  in  phosphorus  poisoning, 
in  diabetes,  in  orthopedic  stretching  operations  on  the 
knee  and  ankle  joints.  In  the  latter  case  there  may  be 
traumatic  epiphyseal  detachment,  and  the  fat  contained 
in  the  spongiosa  would  furnish  material  for  the 
embolus.     In  cases  of  this  kind  considerable  dyspnoea 


6o         DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

may  be  observed  with  small,  frequent  and  weak  pulse, 
hemoptysis  and  cyanosis,  with  complete  consciousness 
until  death,  especially  if  the  status  thymicus  prevail 
as  described  by  Payr.  If  the  fat  particles  pass  through 
the  pulmonary  circulation,  grave  cerebral  symptoms 
may  play  a  prominent  part  from  embolism  of  the  brain. 
Pulmonary  emboli  which  occur  after  reposition  of  in- 
carcerated hemise  and  after  detachment  of  dense  peri- 
typhlitic  adhesions,  are  caused  by  loosening  of  the 
thrombi  in  the  adherent  intestinal  or  peritoneal  veins, 
and  their  migration  through  the  venous  anastomosis 
between  the  portal  vein  and  the  inferior  vena  cava. 

The  most  frequent  cause  of  pulmonary  emboli  is 
primary  coagulations  in  the  right  heart,  mostly  in  the 
right  auricle  and  at  the  tricuspid  valve,  in  rare  cases  at 
the  foramen  ovale,  and  in  the  region  of  the  unclosed 
ductus  arteriosus.  Mention  should  also  be  made  of 
pulmonary  emboli  following  the  entrance  of  air  into 
veins,  as  for  instance,  after  extirpation  of  goitre,  in 
curetting  the  uterus,  and  in  other  surgical  operations. 

Thrombosis  of  the  pulmonary  artery  and  its  branches 
occurs  during  convalescence  after  serious  illness,  in 
cachectic  individuals,  in  tuberculosis,  or  in  conse- 
quence of  compression  of  the  pulmonary  artery  by 
tumors  and  pleuritic  exudates.  These  may  lead  to 
severe  cyanosis  and  dyspnoea  in  the  same  way  as  pul- 
monary emboli,  but  thrombosis  of  several  branches  of 
the  pulmonary  artery  may  at  times,  if  they  develop 
slowly,  remain  latent  without  showing  any  of  these 
symptoms.  If  they  develop  in  the  course  of  diseases 
in  which  there  are  cyanosis  and  dyspnoea,  they  may 


DYSPNCEA   AND   CYANOSIS  6l 

occur  without  materially  intensifying  these  symptoms- 
Thrombosis  during  chlorosis,  observed  in  a  few 
cases,  is  generally  unaccompanied  by  cyanosis.  Latent 
thrombosis  in  pleuritic  exudates  may,  after  evacuation 
of  the  fluid,  lead  to  manifestations  of  a  hemorrhagic 
infarct  and  subsequently  to  death  from  asphyxiation. 

GANGRENE 

In  gangrene  of  the  lungs,  cyanosis  and  dyspnoea 
may  be  accompanied  by  greatly  accelerated  respiration 
which  depends  less  on  the  extent  of  the  gangrene  than 
on  the  original  affection,  and  the  frequent  complication 
with  pleuritis  and  pneumothorax. 

PULMONARY   EMPHYSEMA 

Both  dyspnoea  and  cyanosis  are  among  the  well 
known  symptoms  of  chronic  pulmonary  emphysema. 
The  patient,  when  keeping  quiet,  finds  his  condition 
bearable,  and  dyspnoea  occurs  only  after  bodily 
exertion.  In  spite  of  the  pronounced  dyspnoea,  the 
frequency  of  respiration  is  not  materially  increased, 
unless  there  are  complications  on  the  part  of  the  lung, 
bronchi  or  heart.  Dyspnoea  is  pre-eminently  expira- 
tory, with  distinct  prolongation  of  the  expiration,  and 
the  aid  of  abdominal  pressure  is  needed,  especially  in 
bodily  exertion.  There  is  deficient  expulsion  of  gas 
from  the  pulmonary  alveoli  during  expiration,  in  con- 
sequence of  diminished  elasticity  of  the  lungs  and  in- 
spiratory immobility  of  the  diaphragm.  There  is  also 
insufficient  inspiration,  which  is  responsible  for  the 
type  of  high  thoracic  respiration,  produced  with  the  aid 


62         DISORDERS   OF  RESPIRATION   AND  CIRCULATION 

of  the  inspiratory  auxiliary  muscles  of  the  shoulder. 
The  deeper  the  dyspnoea,  the  more  intense  are  the 
symptoms  on  the  part  of  the  circulation.  The  elastic- 
ity of  the  lungs  assists  in  the  diastolic  dilatation  of  the 
heart,  and  loss  of  this  elasticity  must  diminish  the 
diastolic  filling  of  the  ventricles,  causing  a  stasis  in 
the  capillary  circulation.  This  may  be  responsible  for 
the  cyanosis  which  is  particularly  noticeable  in  in- 
creased muscular  effort. 

If  in  the  further  course,  there  is  obliteration  of  areas 
of  capillaries  in  the  lung  tissue  followed  by  dilatation 
of  the  hypertrophied  right  ventricle,  the  intake  of 
oxygen  into  the  lungs  is  still  further  obstructed,  and 
the  above  symptoms  increase  in  intensity.  When  in- 
efficiency of  the  right  heart  becomes  established, 
cyanosis  is  permanent  and  is  accompanied  by  swelling 
of  the  cervical  veins  which  show  little  or  no  change  in 
volume  on  respiration.  Bronchial  catarrh  favors  the 
development  of  emphysema  and  increases  the  task 
thrown  upon  the  heart. 

There  are  thus  several  factors  to  be  considered  in 
the  causation  of  dyspnoea  and  cyanosis  in  emphysema. 
There  are,  first,  the  primary  changes  in  the  lungs  them- 
selves, then  the  associated  bronchial  catarrh  which  not 
infrequently  displays  the  type  of  asthmatic  bronchitis, 
and  therefore  gives  rise  to  considerable  distress,  and 
finally  secondary  degeneration  of  the  cardiac  muscle. 
An  unusual  event  in  vesicular  emphysema  is  sudden 
dyspnoea  due  to  the  development  of  pneumothorax,  con- 
sequent upon  the  bursting  of  an  emphysematous  vesicle. 
Many  emphysemas  are  the  final  stage  of  bronchial 


DYSPNOEA   AND   CYANOSIS  63 

asthma.  Upon  all  these  conditions  depends  the  char- 
acter of  the  dyspnoea  and  cyanosis,  especially  whether 
the  latter  is  transitory  or  permanent. 

The  preponderance  of  one  of  these  factors  over  the 
others  is  important  for  the  prognosis  and  treatment  of 
emphysema.  Intensity  and  frequency  of  the  accom- 
panying bronchial  catarrh,  and  especially  the  condition 
of  the  heart,  determine  the  prognosis.  The  treatment 
will  differ  according  to  whether  the  diminished  elas- 
ticity of  the  lungs  is  the  primary  affection,  or  whether 
the  bronchitic  factor  predominates,  whether  the  neuro- 
asthmatic  element  is  to  be  taken  into  account,  and 
finally,  whether  the  cardiac  affection,  with  or  without 
simultaneous  arteriosclerosis  dominates  in  the  patho- 
logic picture.  The  pure  form  of  emphysema  requires 
pneumatotherapy,  which,  on  the  other  hand  should  be 
avoided — particularly  expiration  into  rarefied  air — if 
the  bronchitic  element  predominates,  the  latter  requir- 
ing rather  climatotherapy.  The  neuro-asthmatic  type 
of  emphysema  and  the  cardiac  complications  also  re- 
quire therapeutic  individualization.  It  can  be  under- 
stood, therefore,  that  in  emphysema,  the  dyspnoea  will 
be  relieved  in  different  ways,  according  to  the  prepon- 
derance of  one  or  the  other  of  the  above  factors :  one  by 
solanaceous  preparations,  another  by  morphin  and 
oxygen,  a  third  by  iodin  preparations,  others  by  arsenic, 
still  others  by  alkalies  and  diet  (where  gout  is  a 
factor),  and,  finally,  in  emphysema  with  cardiac  com- 
plications, caffein  and  theobromin  preparations  and 
digitalis. 

The  diagnostic  individualization  of  the  purely  pul- 


64         DISORDERS   OF   RESPIRATION   AND  CIRCULATION 

monary,  the  neuro-asthmatic,  the  bronchitic  and  the 
cardiac  factors,  which  is  so  important  for  prognosis 
and  therapy,  is  based  partly  on  physical  findings,  partly 
on  the  examination  of  sputa.  In  eosinophile  catarrh, 
a  genetic  connection  with  asthma  should  be  borne  in 
mind,  and  all  the  symptoms  indicating  the  diagnosis  of 
this  affection  should  be  considered.  The  dry,  moist  or 
muco-purulent  condition  of  the  catarrh  is  important 
for  the  determination  of  the  bronchitic  type.  The 
purely  pulmonary  form  with  decreased  elasticity  of  the 
lungs,  and  resulting  atrophy,  is  at  times  determined, 
aside  from  the  physical  findings  in  the  lungs,  by  the 
behavior  of  the  cenncal  veins.  The  absence  of  inspira- 
tory collapse  in  continued  cyanosis,  shows  that  the  full- 
ness of  the  veins  is  the  same  in  both  phases  of  respira- 
tion. For  the  determination  of  the  condition  of  the 
heart,  all  the  signs  in  cardiac  diagnosis  should  be  ob- 
sePv^ed,  especially  the  area  of  dullness,  which  in  severe 
emphysema  is  diminished  owing  to  the  distended  lung 
encroaching  upon  the  heart,  and  also  from  the  fact  that 
the  left  auricle,  which  materially  influences  the  extent 
of  cardiac  dullness,  is  insuf^ciently  filled  in  emphysema 
in  consequence  of  obliteration  of  pulmonary  capillaries 
and  insufficient  filling  of  the  pulmonary  veins.  The 
cardiac  dullness,  reduced  by  the  dilatation  of  the  lung, 
appears  still  more  contracted  when  compared  with  cases 
of  emphysema  in  which  there  is  mitral  insufficiency, 
mitral  stenosis  or  myocarditic  dilatation  of  the  left 
heart.  The  left  auricle  becomes  dilated  and  increases 
the  cardiac  dullness,  so  that  it  is  distinctly  demonstrable 


DYSPNCEA   AND   CYANOSIS  65 

even  m  emphysema.  In  cases  of  this  kind,  radioscopic 
examination  may  contribute  to  the  understanding  of 
the  case. 

Insufficient  filling  of  the  left  heart  in  extensive 
emphysema  may  cause  systolic  murmurs  in  the  left 
ventricle,  which,  with  hypertrophy  of  the  right  ven- 
tricle, may  give  rise  to  the  mistaken  conclusion  of  a 
mitral  insufficiency  complicating  the  emphysema.  On 
the  other  hand,  a  systolic  cardiac  murmur  may  be  oc- 
casioned by  secondary  relative  tricuspid  insufficiency, 
and  under  these  conditions  it  may  also  be  distinctly 
heard  at  the  apex. 

The  deficient  filling  of  the  left  heart  with  consider- 
able obliteration  of  the  pulmonary  capillaries,  of  course 
leads  to  insufficient  nutrition  of  the  aorta  and  arteries. 
So  long  as  the  right  ventricle  functionates  satisfac- 
torily, this  ischemia  of  the  aortic  system  and  the 
venous  engorgement  of  the  general  circulation  may  be 
compensated,  particularly  if  the  patient  keeps  quiet. 
If  in  emphysema,  muscular  exertion,  such  as  ascending 
stairs,  does  not  produce  noticeable  tachycardia  and 
empty  arteries,  it  may  be  assumed  that  the  right  ven- 
tricle functionates  efficiently,  and  is  capable  of  per- 
forming the  increased  task.  On  the  contrary,  dyspnoea 
and  cyanosis  appearing  under  such  circumstances  in 
conjunction  with  accelerated  and  small  arterial  pulse, 
and  especially  with  signs  of  congested  liver  and  kid- 
ney, would  point  to  inefficient  cardiac  function. 

Dyspnoea  is  also  met  with  in  the  so-called  interstitial 
or  interlobular  form  of  emphysema,  in  which  the  tear- 


66         DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

ing  of  the  pulmonary  alveoli  allows  air  to  enter  into 
the  interlobular  and  then  the  mediastinal  tissue.  In 
infantile  bronchitis  and  pertussis^  or  in  the  presence  of 
foreign  bodies  in  the  air  tract,  interlobular  emphysema 
may  by  compressing  the  pulmonary  alveoli  lead  to  in- 
tense dyspnoea.  Emphysema  in  the  mediastinum  may 
occasion  severe  cyanosis  and  dyspnoea  by  pressure  upon 
the  large  vessels.  The  appearance  of  emphysema  of 
the  skin  in  the  jugular  fossa  and  at  the  neck  is  of 
diagnostic  importance.  In  mediastinitis  postica,  due 
to  the  swallowing  of  foreign  bodies,  as  fish  bones, 
there  is  also  emphysema  of  the  neck  and  face.  The 
dyspnoea,  which  may  be  accompanied  by  fever,  dsy- 
phagia  and  pain  in  the  region  of  the  lower  neck  and 
shoulders,  stands  in  the  foreground  of  the  pathological 
picture. 

ATROPHY  AND    CONTRACTION    OF   THE   LUNGS 

Dyspnoea  and  cyanosis  also  occur  in  atrophy  of  the 
lungs  especially  when  complicated  with  bronchial  ca- 
tarrh, bronchiectasis  and  degeneration  of  the  muscular 
substance  of  the  heart.  The  volume  of  the  lungs  is 
small  and  the  cardiac  dullness  enlarged  only  in  cases 
of  pronounced  atrophy  with  retraction  of  the  lungs, 
the  result  of  considerable  obliteration  of  the  alveoli 
and  capillaries.  An  important  auscultatory  phenome- 
non in  atrophy  of  the  lungs  is  the  peculiar,  hissing 
respiratory  sound,  similar  to  puerile  breathing.  This 
sharp  sound  is  probably  a  transmitted  respiratory  sound 
coming  from  the  non-atrophied  portion  of  the  lung, 
and  in  the  absence  of  other  catarrhal  manifestations 


DYSPNCEA   AND   CYANOSIS  d^ 

is  of  importance  for  the  diagnosis  of  atrophy  of  the 
lungs. 

Secondary  dilatation  and  hypertrophy  of  the  right 
ventricle  are  absent  in  atrophy  of  the  lungs  on  account 
of  the  marasmus.  In  synchronous  arterio-sclerosis  or 
arterio-sclerotic  renal  affections,  hypertrophy  of  the 
left  ventricle  may  occur.  The  diagnosis  may  present 
difficulty  in  cases  where  senile  atrophy  does  not  at- 
tack the  entire  lung  at  the  same  time.  There  is  then 
partial  diminution  of  lung  volume  with  dilatation  of 
the  alveoli  and  deep  position  of  the  diaphragm,  pre- 
senting upon  percussion  the  signs  of  emphysema.  In 
these  cases  it  is  important  to  determine  atrophy  in 
other  organs  as  the  heart  or  liver,  in  order  to  diagnos- 
ticate this  form  of  senile  emphysema.  The  demonstra- 
tion of  an  atrophied  right  ventricle  is  then  of  special 
importance.  The  clinical  picture  of  a  pronounced 
emphysema  with  low  position  of  the  heart  presents 
epigastric  pulsation  as  evidence  of  the  low  position 
of  the  heart  and  of  the  hypertrophy  of  the  right  ven- 
tricle. If  emphysema  with  low  position  of  the  dia- 
phragm can  be  demonstrated  by  percussion  while  epi- 
gastric pulsation  is  absent  in  all  positions  of  the  body, 
that  is  in  standing,  sitting  and  in  ventral  posture,  and 
if  at  the  same  time  serious  fatty  degeneration  of  the 
heart  and  adhesions  to  the  pericardium  can  be  ex- 
cluded, then  the  absence  of  epigastric  pulsation  may 
point  to  atrophy  of  the  heart  and  especially  of  the 
right  ventricle.  In  pulmonary  tuberculosis  complicated 
with  emphysema  and  an  atrophic  heart,  as  in  ane- 


68         DISORDERS  OF  RESPIRATION   AND   CIRCULATION 

mic  tuberculosis,  a  similar  condition  may  be  observed. 
In  these  cases  we  have  to  deal  with  a  kind  o£  atrophy 
from  inactivity  in  consequence  of  the  lessened  quantity 
of  blood  and  therefore  decrease  in  capacity  or  there 
may  be  direct  emaciation  of  the  heart  as  a  part  of  the 
general  emaciation.  In  gout,  too,  I  obsen^ed  this  same 
condition  of  the  heart,  namely  the  absence  of  epigas- 
tric pulsation  with  demonstrable  emphysema.  There 
was  atrophy  of  the  liver  with  stools  deficient  in  bile, 
no  icterus  and  the  diagnosis  of  atrophy  of  the  heart 
and  liver  based  on  these  findings,  was  confirmed  at 
autopsy. 

Dyspnoea  and  cyanosis  are  a  frequent  occurrence  in 
contraction  of  the  lungs,  developed  in  consequence  of 
indurative  pneumonia,  after  influenza  or  pleuritic  exu- 
dates, also  in  the  fibroid  forms  of  phthisis,  in  pul- 
monary syphilis,  anthracosis,  chalicosis,  siderosis  and 
aspergillosis.  In  some  cases  the  proliferation  of  the 
connective  tissue  emanates  from  the  bronchial  and 
mediastinal  glands  which  surround  the  hilus  of  the 
lungs.  This  indurative  periadenitis  may  lead  to  con- 
striction of  the  bronchi  and  the  pulmonary  vessels, 
and  by  extension  to  the  pericardium  produce  adhesion 
of  the  heart  to  the  pericardium,  so  that  in  cases  of  this 
kind  various  factors  contribute  jointly  to  the  produc- 
tion of  dyspnoea  and  cyanosis. 

PULMONARY    SYPHILIS    AND    ACTINOMYCOSIS 

Pulmonary  syphilis  occurring  in  the  form  of  sub- 
acute or  chronic  phthisis  or  simple  chronic  induration 
of  the  lungs,  may  lead  to  dyspnoea  and  cyanosis.   The 


DYSPNCEA  AND   CYANOSIS  69 

dyspnoea  may  attain  a  high  degree,  if  there  is  at  same 
time  stenosis  of  the  upper  air  tract.  The  picture  may 
be  multiform  due  to  diffuse  indurations  of  the  lung, 
the  formation  of  multiple  indurative  foci  of  coarse, 
cicatricial  tissue,  complications  with  adherent  pleuritis 
or  encysted  pleural  exudates,  so  that  it  may  easily  be 
mistaken  for  malignant  tumor,  abscess  of  the  lungs  or 
tuberculosis.  Dieulafoy  specially  refers  to  the  marked 
dyspnoea  in  pleural  exudates  accompanying  pulmonary 
syphilis  and  the  continuance  of  the  same  after  evacua- 
tion of  the  exudate. 

In  actinomycosis  of  the  lungs,  the  occurrence  of 
dyspnoea  and  cyanosis  depends  partly  upon  its  extent 
in  the  lung,  in  part  upon  its  extension  to  the  pleura, 
pericardium,  the  peripleural  connective  tissue  and  the 
thoracic  wall.  If  in  the  further  course  of  pulmonary 
actinomycosis  the  disease  extends  in  different  direc- 
tions and  leads  to  ulceration  with  perforation  of  the 
thoracic  wall,  there  develops  as  a  rule  extensive  ane- 
mia which  in  part  is  also  occasioned  by  the  amyloid 
degeneration  of  the  organs.  Generally  speaking,  there 
is  no  very  severe  dyspnoea  or  cyanosis  in  the  course  of 
actinomycosis,  unless  there  are  special  localizations  of 
the  affection,  as,  for  instance,  miliary  actinomycosis 
of  the  lungs. 

'  TUMORS  OF  THE  LUNGS  AND  BRONCHI 

Severe  dyspnoea  and  cyanosis  may  occur  in  malig- 
nant tumor  of  the  lungs  and  bronchi.  The  dyspnoea 
is  in  part  due  to  the  localization  of  the  new  growth  in 
the  lung  itself  and  its  metastases,  much  more  fre- 


yO         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

quently,  however,  to  its  extension  to  the  mediastinal 
lymphatic  glands.  If  the  larynx  becomes  compressed  or 
if  the  tumor  extends  into  the  larynx,  the  dyspnoea  may 
attain  a  hig-h  degree.  The  clinical  picture  assumes 
different  forms  according  to  whether  pressure  is 
exerted  upon  the  esophagus,  pneumogastric,  recurrent 
laryngeal,  phrenicus  and  symphathicus.  Dyspnoea 
with  or  without  wheezing,  asthmatic  attacks  especially 
at  night,  paralysis  of  the  vocal  cords,  dysphagia, 
vomiting,  tachycardia,  hiccoughs,  hemoptysis,  are  fre- 
quently associated  manifestations.  In  compression  and 
especially  in  thrombosis  of  the  vena  cava,  there  is 
cyanosis  of  the  face  with  marked  engorgement  of  the 
upper  half  of  the  body.  The  vast  majority  of  pa- 
tients succumb  tO'  the  ever  increasing  dyspnoea,  which 
may  even  at  the  onset  of  the  affection — if  the  pleura 
is  affected — be  very  severe  and  as  a  rule  does  not 
subside  after  evacuation  of  the  exudate.  Should  the 
tumors  perforate  into  the  large  vessels  or  the  auricles 
of  the  heart,  the  manifestations  become  exceedingly 
stormy.  In  carcinoma  of  the  lungs  both  dyspnoea  and 
cyanosis  may,  however,  also  be  caused  by  other  and 
non-carcinomatous  affections  of  the  respiratory  organs, 
as  pneumonia,  pleuritis,  or  of  the  organs  of  circulation, 
as  pericarditis,  and  especially  emboli  of  the  pulmonary 
artery  and  thrombosis  of  the  pulmonary  veins.  Siml- 
larily,  other  malignant  and  benign  tumors  of  the  lung, 
sarcoma,  enchondroma,  lipoma,  fibroma,  osteoma,  der- 
moid cysts  and  echinococci,  may  by  compression  of  the 
air  tract  and  the  large  vessels  as  well  as  by  complica- 


DYSPNCEA   AND   CYANOSIS  7 1 

tions  produce  cyanosis  and  dyspnoea.  Grave  dyspncea 
has  been  observed  in  emboli  of  the  pulmonary  artery 
with  echinococci  in  consequence  of  the  perforation  of 
a  subendocardial  colony  into  the  interior  of  the  right 
ventricle  of  the  heart. 

Emboli  of  the  pulmonary  artery  which  have  been 
found  in  neoplasms  of  the  adrenals  are  of  special  im- 
portance. New  growths  of  the  adrenals  may,  as  is 
well  known,  grow  into  the  adrenal  vessels,  the  renal 
vein  and  the  vena  cava  superior.  These  growths  may 
then  become  detached  and  cause  sudden  death  by  em- 
bolism of  the  pulmonary  artery.  Such  a  result  hap- 
pened at  an  operation  for  a  renal  tumor  during  the 
anesthesia.  The  gravest  dyspnoea  with  violent  cough- 
ing and  cyanosis  occurs  if  echinococci  break  into  the 
lungs.  *■ 

TUBERCULOSIS 

In  tuberculosis  of  the  lungs,  cyanosis  and  dyspnoea 
are  usually  not  common  symptoms.  In  advanced 
phthisical  cases,  dyspncea  and  cyanosis  are  frequently 
absent,  although  there  is  present  extensive  infiltration 
of  the  lungs  and  considerable  difficulty  in  respiration 
as  in  pneumothorax.  In  spite  of  the  diminution  of  the 
area  for  respiration  on  account  of  the  progressive  de- 
struction of  the  lungs,  most  phthisical  patients  do  not 
experience  any  subjective  dyspnoea,  although  the  fre- 
quency of  respiration  increases.  The  absence  of  dysp- 
noea and  cyanosis  is  usually  attributable  to  the 
autoconsumption  of  the  patients  and  is  explained  by 
the  quantitative  impoverishment  of  the  blood  in  red 


^2         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

blood  corpuscles,  which,  by  g'iving-  up  oxygen  in  the 
capillaries,  produce  the  characteristic  venous  blood. 

The  appearance  of  intense  dyspnoea  in  phthisical 
subjects  is  therefore  an  accessory  phenomenon  g'iving 
rise  to  the  suspicion  that  the  primary  affection  has  been 
complicated  by  some  severe  disturbance  of  the  circula- 
tion or  respiration.  In  some  cases  it  is  an  acute  lar}^n- 
geal  stenosis  from  perichondritis,  or  edema  of  the  glot- 
tis, and  is  accompanied  by  dyspnoea,  wheezing  and 
hoarseness.  But  the  respirator}^  obstruction  may  lie 
deeper  and  be  caused  by  a  bronchial  stenosis,  in  conse- 
quence of  compression  by  tubercular  or  ulcerative 
glands  or  by  a  pseudo-membranous  bronchitis,  as  oc- 
curs in  tubercular  bronchial  tumors.  In  other  cases 
the  cause  is  to  be  found  in  an  acutely  developing  dif- 
fuse bronchitis,  in  mixed  infections  with  the  influenza 
bacillus  and  this  may  be  determined  by  the  bacterio- 
logical examination  of  the  sputum.  In  children  espe- 
cially, both  dyspncea  and  cyanosis  may  be  ver}^  intense 
by  the  addition  of  capillar}'-  bronchitis.  In  these  cases 
the  possibility  of  redevelopment  of  military  tuber- 
cles should  also  be  kept  in  mind,  especially  if  in 
the  course  of  tuberculosis  with  comparatively  slight 
bronchial  manifestations  there  is  considerable  cya- 
nosis, marked  increase  in  the  frequency  of  respiration 
and  pulse  with  unimportant  subjective  dyspnoea,  but 
with  high  fever,  impairment  of  consciousness  and  in- 
creasing loss  of  vitality. 

In  high  fever,  the  increased  difficulty  in  breath- 
ing may  also  be  caused  by  the  fact  that  the  primary 


DYSPNCEA   AND   CYANOSIS  73 

affection  is  complicated  by  a  pneumococcic  infection, 
in  which  case  the  sputum  assumes  the  characteristic 
properties  o£  pneumonic  sputum,  and  the  physical 
manifestations  of  pneumonia  occupy  the  more  promi- 
nent place.  In  this  rusty-colored  sputum  there  are 
then  not  only  tubercle  bacilli  demonstrable,  but  in  the 
beginning  of  the  affection  also  the  diplococcus  of  pneu- 
monia, which  under  the  microscope  appear  often  as 
encapsuled  cocci.  Where  the  capsule  is  missing,  their 
virulence  is  demonstrable  on  test  animals  from  the  pure 
culture  obtained  from  the  sputum.  In  these  cases  the 
dyspnoea  can  in  part  be  traced  to  the  acute  reduction 
of  the  area  of  respiration,  and  partly  also  to  toxic 
influences  from  the  mixed  infection.  This  mixed  in- 
fection, which  should  be  regarded  as  a  diplococcus 
pneumonia,  is  characterized  by  special  changes  in  the 
blood  and  by  its  comparatively  acute  course.  There 
are  also  forms  of  tubercular  pneumonia  occasioned  by 
reinfection  with  the  tubercle  bacillus  itself,  in  which 
rusty-colored  sputa,  bronchial  breathing  and  crepitant 
rales  simulate  the  picture  of  a  fibrinous  pneumonia. 
These  forms  which  A.  Fraenkel  designates  as  pneu- 
monic forms  of  acute  pulmonary  tuberculosis  usually 
lead  to  caseation,  in  rarer  cases  to  extensive  indura- 
tion, bronchial  dilatation  and  indurative  adhesions  of 
the  pleura.  They  generally  progress  with  continuous 
dyspnoea,  while  cyanosis  is  less  prominent  in  the  patho- 
logical picture  in  consequence  of  the  progressive  ane- 
mia and  the  low  state  of  nutrition  unless  special  com- 
plications are  present, 


74         DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

In  mixed  streptococcic  infections,  dyspnoea  may  be 
met  with,  especially  in  cases  where  ulcerative  pleu- 
ritis  and  pericarditis  occur  in  the  course  of  pulmonary 
tuberculosis.  This  is  true  not  only  of  ulcerations  of 
the  peribronchial  and  mediastinal  lymphatic  glands, 
but  also  of  those  rare  cases  of  ulcerative  peribronchitis 
which  emanate  from  the  smallest  branches,  extend  up- 
ward along  the  lymphatics  to  the  region  of  the  bronchi 
and  lead  to  ulceration  of  the  bronchi  and  pulmonar}^ 
parenchyma^  causing  death  with  the  picture  of  acute 
septicemia.  In  all  these  bronchitic,  pneumonic  and 
peribronchitic  forms  of  pulmonary  tuberculosis,  cya- 
nosis and  difficulty  in  breathing  may  occur  in  the  early 
and  non-anemic  cases,  when  constriction  of  the  bronchi 
and  reduction  in  the  area  of  respiration  acutely  in- 
terferes with  the  interchange  of  pulmonary  gases. 

In  the  pleuritic  form  of  pulmonary  tuberculosis 
with  insidious  development  of  the  exudate  the  occur- 
rence of  great  difficulty  in  breathing  and  cyanosis  is 
not  commonly  obsen-ed.  The  absence  of  these  symp- 
toms is  explained  by  the  anemia  of  the  patient  which 
is  present  at  the  beginning  of  the  pleuritis.  If  in  such 
cases,  dyspnoea  nevertheless  makes  its  appearance,  it 
is  occasioned  either  by  pain  and  pleural  stitches,  es- 
pecially when  the  exudates  develop  rapidly,  by  the  de- 
velopment of  exudates  in  encysted  spaces,  or  by  a 
special  localization  of  the  exudates  as  in  diaphragm- 
atic pleuritis. 

In  adhesions  of  the  pleurae,  the  dyspnoea  may  re- 
semble the  picture  of  asthma  or  simulate  an  emphy- 


DYSPNCEA   AND   CYANOSIS  75 

sema  of  the  lungs,  if  patients  are  constrained  by  ad- 
hesions and  immobilization  of  the  diaphragm  to 
breathe  with  the  upper  chest.  By  overlooking  the 
primary  affection,  the  therapy  may  be  entirely  wrong. 
It  is  therefore  not  superfluous  to  point  out  that  in  cases 
of  emphysema  or  asthma  which  are  not  quite  clear, 
the  most  careful  examination  of  the  sputum  for  the 
presence  of  tubercle  bacilli  may  be  decisive.  The  speci- 
men should  be  prepared  by  centrifugating  a  large 
quantity,  and  it  may  also  be  inoculated  into  guinea 
pigs.  I  know  of  a  case  which  had  been  treated 
for  a  considerable  time  as  asthma  in  pneumatic  cab- 
inets until  a  rather  profuse  hemoptysis  resulted.  This, 
together  with  the  history  of  pleuritis  and  the  finding 
of  the  tubercle  bacilli  in  the  sputum,  which  contained 
no  eosinophile  cells,  revealed  the  true  nature  of  the  af- 
fection. It  should  also  be  mentioned  that  there  are 
combinations  of  pulmonary  tuberculosis  with  bronchial 
asthma,  the  tuberculosis  developing  in  patients  who 
formerly  suffered  or  still  suffer  from  typical  asthmatic 
paroxysms.  I  remember  a  case  where  in  the  sputum 
not  only  numerous  tubercle  bacilli  were  found, 
but  also  eosinophile  cells  and  Charcot's  crystals.  A 
stay  in  the  mountains  was  followed  by  a  considerable 
aggravation  of  the  condition  and  an  exacerbation  of 
the  asthmatic  paroxysms.  In  rare  cases  asthmatic  at- 
tacks are  observed  in  tuberculosis  immediately  after 
the  injection  of  tuberculin.  The  sputum  in  these  cases 
contained  eosinophile  cells  and  Charcot's  crystals,  and 
the  blood  too  showed  eosinophile  cells  in  great  abun- 


76         DISORDERS   OF   RESPIRATION   AND  CIRCULATION 

dance.  In  the  sputum  of  tuberculous  women  the 
eosinophile  cells  sometimes  undergo  a  surprising  in- 
crease at  the  time  of  menstruation.  As  menstruation 
in  the  development  of  temperature  acts  similarly  to  a 
tuberculin  injection,  it  is  possible  that  both  premen- 
strual dyspnoea  and  the  above  findings  in  the  sputum 
should  be  regarded  from  the  same  standpoint,  as  due 
perhaps  to  a  toxic  influence. 

A  not  infrequent  cause  of  the  sudden  development 
of  dyspnoea  in  pulmonary  tuberculosis  is  pneumo- 
thorax, but  in  the  vast  majority  of  cases  cyanosis,  as 
well  as  dyspnoea,  does  not  appear  at  all  or  is  only 
slightly  indicated,  especially  when  the  pneumothorax 
develops  in  a  circumscribed  area,  or  from  a  perfora- 
tion of  a  severely  affected  lung  incapable  of  respira- 
tion. If,  however,  dyspnoea  exists  to  an  extent  to 
cause  anxiety,  it  should  be  considered  as  a  prognosti- 
cally  serious  symptom.  It  is  caused  by  a  pneumo- 
thorax occurring  in  the  less  diseased  lung  while  the 
other  lung  is  severely  affected. 

In  some  cases  of  pulmonary  tuberculosis  the  dysp- 
noea may  be  occasioned  by  glands  compressing  the 
pneumogastric  nerve,  and  occurs  not  infrequently  in 
paroxysmal  attacks  with  violent  coughing,  defying  all 
treatment.  Furthermore,  dyspnoea  may  occur  paroxys- 
mally  with  rapid  elevations  of  temperature,  particu- 
larly when  the  nightly  exacerbations  of  fever  take 
place.  It  is  attributable  less  to  the  effect  of  the  toxins 
and  rather  to  the  temperature,  as  after  the  administra- 
tion of  antipyretics  and  the  reduction  of  fever  by 


DYSPNCEA   AND   CYANOSIS  jy 

phenacetin,  quinin  or  hydropathic  measures,  sponging 
with  vinegar,  the  dyspnoea  promptly  subsides. 

In  afebrile,  chronic,  pulmonary  tuberculosis  also, 
dyspnoea  and  cyanosis  may  occur.  These  forms  are 
designated  as  phthisis  fibrosa,  and  their  frequent  com- 
plications— emphysema,  pleural  adhesions,  especially 
adhesions  of  the  heart  to  the  pericardium — cause  the 
disturbances  of  respiration  to  take  such  a  prominent 
place  as  to  present  the  affection  rather  under  the 
picture  of  cardiac  inefficiency.  These  forms  some- 
times lead  to  hypertrophy  and  dilatation  of  the  right 
ventricle,  and  the  final  phase  of  the  affection  may 
appear  under  the  mask  of  a  tricuspid  insufficiency. 

In  ordinary  pulmonary  tuberculosis  dyspnoea  and 
cyanosis  of  varying  degree  may  be  present  in  conse- 
quence of  pericarditis  or  of  changes  in  the  heart  itself, 
as  in  fatty  degeneration  of  the  muscular  substance. 
The  pericardial  adhesions,  which  are  so  frequent  in 
tuberculosis,  deserve  special  attention,  because  they 
may,  not  infrequently,  be  the  cause  of  a  fatal  edema 
of  the  lungs.  I  have  myself  observed  a  case  of  tuber- 
culosis complicated  by  a  pleural  exudate,  where  im- 
mediately after  evacuation  of  the  exudate  there  was  an 
improvement  in  the  dyspnoea.  The  patient  felt  better, 
but  after  a  few  hours  a  high  degree  of  dyspnoea  with 
albuminous  expectoration  occurred,  leading  to  a  fatal 
termination  with  symptoms  of  pulmonary  edema. 
Cases  have  been  rarely  observed,  where  patients  ex- 
tremely dyspnoeic,  unconscious,  with  small  and  often 
irregular  pulse,  presenting  a  moribund  appearance,  re- 


78         DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

covered  rapidly  and  completely,  only  to  succumb  to  a 
fresh  recurrence  of  the  attack.  The  autopsy  in  these 
cases  revealed  tuberculosis  of  the  heart  muscle. 

One  of  the  more  frequent  causes  of  grave  and  sud- 
denly developing  dyspnoea  and  cyanosis  in  tuberculosis 
is  embolus  of  the  pulmonary  artery  from  thrombosis 
of  the  peripheral  veins.  Dyspnoea  and  cyanosis  also 
occur  in  those  forms  of  pulmonary  tuberculosis  which 
develop  secondarily  in  a  pre-existing  cardiac  insuffi- 
ciency, as  congenital  mitral  stenosis  or  affections  of 
the  pulmonary  valves,  and  especially  in  aneurisms 
of  the  thoracic  aorta.  This  is  also  true  of  tuberculosis 
in  kyphoscoliosis  where  the  tuberculosis  develops  in 
those  sections  of  the  lung  which  are  poorly  nourished 
owing  to  the  deformity.  In  caries  in  the  region  of 
the  fourth  cer\ncal  verebra  severe  dyspnoea  may  occur 
when  the  affection  spreads  to  the  nucleus  of  the  phren- 
icus  and  is  followed  by  paralysis  of  the  diaphragm. 

Intense  dyspnoea  with  violent  paroxysms  of  suffoca- 
tion may  occur  in  tuberculosis  through  the  erosion 
of  small  aneurisms  or  of  large  blood  vessels  into 
cavities.  Cases  where  ulcerative  tuberculous  glands 
break  through  into  the  pericardium  or  aorta  may  be 
mentioned  as  rarities. 

Furthermore,  dyspnoea  is  found  when  tuberculosis 
is  complicated  with  nephritis,  especially  in  cases  where 
the  blood  pressure  is  raised.  As  is  well  known,  most 
cases  of  advanced  tuberculosis  have,  as  a  rule,  a  low 
blood  pressure,  but  where  there  is  coincident  nephritis, 
this  rule  usually — but  not  always — shows  an  excep- 


DYSPNOEA   AND    CYANOSIS  79 

tion,  and  this  refers  especially  to  cases  which  have  a 
pronounced  tendency  to  dyspnoea  and  chronic  edema 
of  the  lungs. 

Finally  there  is  the  dyspnoea  of  tuberculosis  com- 
plicated with  hysteria  or  neurasthenia.  A  tubercu- 
lous female  patient  in  our  clinic  had  paroxysms  of 
dyspnoea  at  times  during  the  day,  especially  when  she 
knew  she  was  being  observed,  and  these  paroxysms 
bore  the  precise  character  of  hysterical  tachypnoea. 
To  this  group  also  belong  those  forms  of  paroxysmal 
dyspnoea  experienced  most  frequently  at  night  in  neu- 
rotic and  neurasthenic  patients.  These  cases  have 
been  cited  by  See  and  A.  Fraenkel  as  examples  of  so- 
called  pseudo-asthma. 

PLEURAL  EXUDATES 

In  pleural  exudates,  dyspnoea  occurs  coupled  with 
cyanosis.  These  phenomena  depend  less  on  the  size 
of  the  exudate  than  on  the  rapidity  with  which  it  de- 
velops, partly  also  on  the  nature  of  the  causative  fac- 
tor and  on  the  concomitant  and  original  pathological 
conditions.  There  are  cases  of  exudative  pleuritis 
which  are  ushered  in  with  repeated  chills,  at  times 
accompanied  by  high  fever  and  sometimes  by  expec- 
toration of  bloody  sputum.  This  stormy  introduction 
characterizes  especially  suppurative  pleuritis  and  the 
exudate  may  develop  with  such  rapidity  as  to  necessi- 
tate its  evacuation  within  a  few  days.  These  forms 
simulate  the  picture  of  pleuro-pneumonia  and  may  give 
rise   to   a   wrong   diagnosis   of   genuine   pneumonia. 


8o         DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

Dyspnoea  and  especially  cyanosis  have  considerable 
diagnostic  significance,  as  the  latter  is  usually  a  late 
symptom  in  genuine,  uncomplicated  pneumonia.  In 
very  large  exudates  there  is  deep  cyanosis  of  the  whole 
body  in  consequence  of  the  severe  disturbances  of 
circulation  due  to  the  limitation  of  the  thoracic  space, 
and  there  is  besides  edema  of  the  ankles  and  later 
general  dropsy.  i\Iarked  dyspnoea  and  cyanosis  also 
occur  in  comparatively  small  exudates,  if  they  are 
mediastinal,  and  when  there  is  also  pronounced  inter- 
lobular empyema. 

Intrathoracic  carcinoma  and  sarcoma  causing  effu- 
sion into  the  pleural  space  may,  as  mentioned  before, 
produce  or  increase  cyanosis  and  dyspnoea  by  enlarge- 
ment of  the  glands  and  compression  of  the  vena  cava, 
of  the  pulmonary  artery  and  veins,  or  by  the 
direct  extension  of  the  growth  to  the  walls  of 
the  vessels,  with  resulting  thrombosis  and  embolism. 
Such  thrombi  in  the  branches  of  the  pulmonary  veins 
may  be  carried  into  the  general  circulation,  especially 
on  evacuation  of  the  exudate.  In  other  cases  dyspnoea 
is  coupled  with  anemia  and  especially  in  malignant 
neoplasms  with  bloody  effusions  in  the  pleural  cavity. 
The  persistence  of  dyspnoea  or  only  its  slight  relief 
after  evacuation  of  the  effusion  from  the  pleural  cavity 
in  the  case  of  a  carcinoma  has  already  been  mentioned. 

Cyanosis  and  dyspnoea  in  pleuritis  may,  aside  from 
the  quantity  of  the  exudate,  attain  a  high  degree  ow- 
ing to  the  accompanying  paralysis  of  the  diaphragm, 
especially  in  pleuritis  diaphragmatica,  where  violent 


DYSPNCEA   AND    CYANOSIS  51 

diaphragmatic  pains  and  involvement  of  the  pericar- 
dium play  a  part. 

In  combination  with  concomitant  or  pre-existing  af- 
fections of  the  heart  and  kidney,  dyspnoea  may  be  in- 
tensified to  orthopnoea.  The  patient  has  to  sit  up  in 
bed  in  order  to  remove  from  the  lungs  the  exudate 
accumulated  at  the  base  of  the  lungs. 

The  gravest  form  of  dyspnoea  may  occur  from  per- 
foration of  the  pleural  space  by  echinococci.  The 
dyspnoea  constantly  and  at  times  rapidly  increases, 
and  is  generally  the  prominent  symptom  of  intratho- 
racic echinococci.  Death  from  suffocation  is  not  a  rare 
occurrence  in  contradistinction  to  pleuritic  exudates. 
Test  punctures  of  the  pleural  and  pulmonary  echino- 
cocci may  be  followed,  in  addition  to  urticaria,  by 
grave  conditions  of  collapse.  There  may  be  death 
from  suffocation  if  the  sac  should  rupture  and  the 
contents  of  the  cysts  should  occlude  the  respiratory 
tract. 

In  contradistinction  to  this  grave  dyspnoea  and  cya- 
nosis, after  effusion  and  perforation  into  the  pleura, 
there  are  numerous  cases,  not  only  of  moderate  but 
also  of  large  exudates,  in  which  there  is  complete  ab- 
sence of  dyspnoea  or  cyanosis  and  especially  if  there 
is  no  fever  and  the  patient  lies  quietly  in  bed.  The 
least  physical  exertion,  sitting  up  or  rising,  may  pro- 
duce considerable  difficulty  in  breathing  and  cyanosis. 
The  cause  of  these  attacks  varies:  kinking  of  the 
trachea  or  of  the  vena  cava;  weakness  or  thrombosis 
of  the  heart;  pulmonary  edema;  perforation  of  an 


82         DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

exudate  into  the  lungs,  mediastinum  or  pericardium. 
Difficulty  in  breathing-  may  also  occur  in  slight  exu- 
dates, if  the  pleuritis  develops  in  encysted  spaces, 
walled  off  by  former  adhesions.  The  dyspnoea,  which 
not  infrequently  is  associated  with  pains  in  the  affected 
side  of  the  chest,  is  caused  by  the  impediment  to  res- 
piration and  circulation,  formed  by  the  adhesions 
and  complicated  by  the  space-restricting  pleuritic 
effusion. 

Similarly,  cyanosis  and  dyspnoea  occur  In  total  ad- 
hesion of  the  pleural  layers.  As  the  adherent  limg 
cannot  expand  in  its  vertical  diameter,  the  thorax  is 
forced  to  undergo  more  than  normal  expansion  in  the 
frontal  and  sagittal  diameters,  and  hence  the  costal 
type  of  respiration  as  it  exists  in  emphysema  of  the 
lungs.  The  adhesion  of  the  pleural  layers  follows  pleu- 
ritis in  the  course  of  chronic  tuberculosis.  The  pleu- 
ritis is  not  infrequently  only  a  part  manifestation  of  a 
general  serositis,  and  in  consequence  of  simultaneous 
adhesions  of  the  pericardial  layers,  of  the  diaphragm 
and  liver,  the  clinical  picture  may  have  multiform  fea- 
tures. The  dilatation  of  the  thorax  in  pleural  ad- 
hesions recalls  that  of  emphysema.  The  protracted 
expiration,  the  asthmatic  paroxysms  and  the  hyper- 
trophy of  the  right  ventricle  are  apt  to  cause  difficulty 
in  the  differential  diagnosis  of  both  affections.  Secon- 
dary bronchial  catarrh  develops  in  the  poorly  nourished 
portions  of  the  lung,  and  like  emphysema,  may  lead 
to  dilatation  of  the  right  ventricle,  which  may  become 
distended  enough  to  cause  a  relative  tricuspid  insuf- 


DYSPNCEA  AND   CYANOSIS  83 

ficiency.  Both  cyanosis  and  dyspnoea  may  then  attain 
a  very  intense  degree,  especially  if  there  is  simultane- 
ous adhesion  of  the  pericardium  to  the  heart  and 
weakness  of  the  heart,  especially  of  the  right  ven- 
tricle. 

PNEUMOTHORAX,  PYO-PNEUMOTHORAX 

Pneumothorax  leads  to  dyspnoea  and  cyanosis  only 
if  the  collapsed  lung  was  not  previously  materially  af- 
fected or  in  good  functionating  condition,  as  happens 
in  stabbing  and  shooting  wounds  and  in  emphysema. 
The  lung  not  only  of  the  affected,  but  also  of  the  op- 
posite side  becomes  retracted,  from  the  entrance  of 
air  into  the  thoracic  space.  The  mediastinum  is  then 
displaced  if  it  be  pliable  and  unaffected.  If  it  contains 
indurative  tissue  and  if  the  lung  on  the  side  of  the 
pneumothorax  is  partially  adherent  to  the  thoracic 
wall,  then  the  healthy  side  will  be  less  impeded  in  its 
movements  than  when  the  respiratory  organs  are  rela- 
tively healthy.  On  these  factors  then:  the  condition 
of  the  lung  on  the  side  of  the  pneumothorax,  the  be- 
havior of  the  mediastinum  and  of  the  opposite  lung, 
depends  the  occurrence  of  dyspnoea  in  pneumothorax. 

When  speaking  about  dyspnoea  in  tuberculosis,  ref- 
erence was  made  to  the  fact  that  dyspnoea  is  absent  or 
only  faintly  indicated  when  the  pneumothorax  is 
circumscribed  or  has  followed  the  perforation  of  a 
seriously  affected  lung  adherent  to  the  pleura  and  there- 
fore useless  for  purpose  of  respiration.  If,  on  the  con- 
trary, pneumothorax  occurs  on  the  side  of  the  less 


84        DISORDERS    OF    RESPIRATION    AND    CIRCULATION 

affected  lung  with  a  seriously  affected  lung  opposite, 
there  may  be  the  most  intense  dyspnoea  leading  to 
sudden  death  from  asphyxiation.  These  sudden 
deaths  in  pneumothorax  occur  in  cases  where  the  pul- 
monary changes  are  not  marked  or  where  there  is  a 
quiescence  in  their  further  development.  They  are 
fully  explained  by  the  mechanism  of  pneumothorax 
and  the  rapid  functional  collapse  of  the  lungs.  The 
condition  of  the  pulmonary  fistula  may  also  come  into 
question.  In  the  case  of  a  closed  or  valvular  pneu- 
mothorax the  retraction,  and  therefore  also  the 
dyspnoea,  may  attain  an  intense  degree  in  consequence 
of  the  high  positive  pressure  in  the  pleural  cavity, 
while  in  an  open  pneumothorax,  unless  it  is  bilateral 
as  may  be  the  case  in  penetrating  chest  wounds, 
dyspnoea  may — ceteris  paribus — not  be  present  at 
all  or  only  moderately,  and  the  want  of  oxygen  be 
supplied  by  more  rapid  and  deeper  respiration.  In 
simultaneous  effusion  of  fluid,  that  is  in  pyo-pneu- 
mothorax,  the  increase  of  the  exudate  and  its  char- 
acter is  of  some,  but  not  of  much  importance. 

In  penetrating  shot  wounds  of  the  chest  which  open 
the  pleural  cavity  dyspnoea  and  cyanosis  are  common 
manifestations.  In  shots  entering  the  lungs  hemop- 
tysis is  a  constant  symptom  in  addition  to  those  of 
pneumothorax.  An  interlobular  and  mediastinal 
emphysema  increases  the  dyspnoea,  and  may,  if  its  on- 
set is  rapid,  lead  to  death  from  suffocation.  While 
dyspnoea  and  hemoptysis  constitute  the  most  important 
signs  of  injuries  to  the  pleura  and  lungs,  cyanosis  may 


DYSPNCEA   AND    CYANOSIS  85 

be  completely  absent,  and  anemia — in  addition  to  the 
dyspnoea — may  prevail  in  cases  where  an  important 
vessel  has  been  injured.  As  the  hemorrhage  con- 
tinues, the  patient  becomes  more  and  more  anemic,  the 
pulse  smaller,  the  respiration  superficial,  and  in  this 
condition  death  often  occurs  from  synocope. 

SCOLIOSIS 

Dyspnoea  in  scoliosis  may  be  caused  in  different 
ways.  It  may  be  occasioned  by  pressure,  atrophy  of 
the  lungs  and  the  impossibility  of  distending  the 
thorax.  This  results  in  a  compensatory  acceleration 
of  respiration  attended  by  almost  exclusively  abdomi- 
nal breathing  as  long  as  the  right  ventricle  function- 
ates sufficiently.  If  the  latter  fails,  the  deficient 
distention  and  contraction  of  the  pulmonary  alveoli 
may  cause  insufficient  circulation  in  the  lung  and 
interchange  of  gases,  and  dyspnoea  is  the  result  of 
the  oxygen  famine.  This  dyspnoea  is  based  on  the 
diminished  quantity  of  blood  transmitted  into  the  cir- 
culation and  materially  differs  from  the  dyspnoea  of 
engorgement  where  the  lungs  are  overfilled  with 
blood,  which  flows  under  high  pressure  into  the 
dilated  left  auricle.  The  former  receives  less  blood 
from  the  pulmonary  veins,  and  thus  both  the  left 
auricle  and  the  left  ventricle  are  frequently  found 
small  and  atrophic. 

This  condition,  however,  is  by  no  means  the  rule  in 
scoliosis.  There  are  cases  of  kyphoscoliosis  with  cya- 
nosis, enlargement  of  the  liver  and  dropsy  from  venous 


86        DISORDERS    OF    RESPIRATION    AND    CIRCULATION 

obstruction,  in  which  the  absence  of  dyspnoea  is  a 
surprising  contradiction.  These  patients  can  lie  on 
their  backs  or  even  sit  up  in  bed  without  experiencing 
distress  or  dyspnoea.  This  reminds  one  of  cases  with 
congenital  insufficiency  of  cardiac  function.  I  have 
seen  a  patient  suffering  from  kyphoscoliosis  with  con- 
siderable edema  of  the  lower  extremities,  who  dis- 
played this  surprising  contradiction  of  symptoms  as 
long  as  his  pulse  was  good  and  the  action  of  the  left 
ventricle  sufficient.  To  explain  the  cyanosis  in  these 
cases,  it  is  necessary  to  assume  that  the  right  ventricle 
is  comparatively  weak,  and  as  the  left  ventricle  is 
strong,  no  dyspnoea  develops,  but  only  symptoms 
of  passive  congestion  in  the  general  circulation.  If, 
however,  the  left  ventricle,  too,  becomes  inefficient,  if 
the  pulse  is  weak,  frequent  and  irregular,  then  there 
is  added  to  the  passive  congestion  of  the  circulation  an 
engorgement  of  the  pulmonic  circulation  which  finds 
expression  in  dyspnoea  with  asthmatic  attacks.  Ley- 
den  has  already  pointed  to  the  functional  differences 
between  the  right  and  left  ventricles  in  his  work  on 
the  fatty  heart.  I  lay  special  stress  upon  these  cases, 
because  they  are  of  interest  from  both  a  prognostic 
and  therapeutic  point  of  view.  The  point  to  which 
treatment  is  to  be  directed  is  not  improvement  of  car- 
diac function,  but  relief  of  the  work  performed  by  the 
general  circulation,  by  deflection  to  the  intestines,  by 
diuresis  or  venesection.  It  is  a  struggle  between  the 
right  ventricle  and  the  diminished  area  of  respiration 
in  the  pulmonic  circulation,  while  the  left  ventricle  is 


DYSPNOEA   AND    CYANOSIS  8/ 

involved,  only  as  it  may  be  expected  to  perform 
increased  work  owing  to  the  engorgement  of  the  venous 
capillaries.  If,  however,  the  left  ventricle  also  be- 
comes exhausted,  there  will  be  a  dyspnoea  similar  to 
cardiac  asthma,  to  which  more  explicit  reference  will 
be  made  later  on. 


PART  II 

DYSPNCEA   AND    CYANOSIS    IN    DIS- 
ORDERS OF  THE  CIRCULATION 


DYSPNCEA  AND  CYANOSIS  IN  CONGENITAL 
CARDIAC  LESIONS 

In  the  beginning  it  was  explained  that  in  affections 
of  the  respiratory  system  dyspnoea  was  a  frequent 
manifestation,  and  that  the  associated  cyanosis  was,  in 
the  great  majority  of  cases,  attributable  to  complica- 
tions from  cardiac  insufficiency,  or  else  to  grave  dis- 
turbances in  the  interchange  of  gases  in  the  lungs. 
In  affections  of  the  circulation,  the  majority  of  cases 
of  dyspnoea  are  complicated  by  more  or  less  pronounced 
cyanosis  of  all  degrees  of  intensity,  from  pure  blue  to 
blue  black. 

The  most  marked  grades  of  general  cyanosis  occur 
In  congenital  cardiac  insufficiency,  and  as  a  rule  exist 
from  birth  or  earliest  infancy.  In  acquired  cardiac  de- 
fects cyanosis  never  attains  so  high  a  degree  and  runs 
to  a  certain  extent  a  course  parallel  to  the  intensity  of 
of  the  subjective  symptoms,  especially  the  dyspnoea. 
It  is  usually  a  late  symptom  and  generally  accompa- 
nies the  dropsy.  Congenital  cardiac  defects  some- 
times show  a  striking  contrast  between  the  extent  of 
cyanosis  and  the  subjective  symptoms,  especially 
the  dyspnoea.  Persons  suffering  from  the  most  intense 
cyanosis  may  be  able  to  perform  heavy  work  with- 

91 


92         DISORDERS   OF   RESPIRATION  AND  CIRCULATION 

out  loss  of  breath.  These  are,  however,  exceptional 
cases,  and  usually  cyanosis  is  accompanied  by  dysp- 
noea which  may  be  severe  enough  to  threaten  suffo- 
cation. Nevertheless,  cyanosis  in  congenital  cardiac 
defects,  whether  it  has  existed  from  earliest  infancy  or 
has  gradually  increased,  occupies  the  foreground  of  the 
clinical  picture.  It  is  also  surprising  that  in  many  con- 
genital forms  of  cyanosis  the  small  peripheral  veins  are 
dilated  to  the  utmost,  while  the  large  veins  show  no 
distention,  and  there  is  frequently  a  disproportion 
between  the  cutaneous  cyanosis  and  the  stasis  in  the 
internal  organs.  In  acquired  cardiac  defects  edema 
precedes  severe  cyanosis,  or  at  least  accompanies  it, 
while  the  opposite  holds  good  for  congenital  lesions, 
and  edema  occurs  late  or  not  at  all.  The  absence  of 
pronounced  congestions  of  the  internal  organs  and  also 
of  dropsy,  in  spite  of  the  most  intense  cyanosis,  may 
possibly  be  explained  by  structural  changes  with  disten- 
tion of  the  superficial  capillaries  and  by  hypertrophy 
of  the  veins  with  their  adaptation  to  the  slowly 
developing  overpressure. 

In  congenital  valvular  defects,  cyanosis  may  make  its 
appearance  in  intercurrent  affections  which  weaken  the 
circulation,  as  scarlet  fever,  measles,  whooping  cough, 
typhoid  and  pulmonary  affections.  Other  factors,  as 
pregnancy,  which  increase  the  demand  upon  the  heart, 
may  produce  the  same  effect,  and  lead  later  to  cyanosis. 
In  some  cases  there  is  transitory  cyanosis  in  crying  or 
coughing  spells,  or  after  bodily  exertion.  It  may  be- 
come  permanent   when   there   is    inefficiency   of   the 


DYSPNCEA   AND   CYANOSIS  93 

cardiac  muscle,  or  there  are  changes  in  the  lungs, 
especially  in  the  pulmonary  vessels.  Even  when 
cyanosis  has  been  caused  by  factors  interfering  with 
the  circulation,  there  is  often  considerable  dispropor- 
tion between  the  cyanosis  and  the  causative  factor,  as 
bronchitis.  From  a  diagnostic  point  of  view,  there- 
fore, the  appearance  of  cyanosis  in  the  course  of  slight 
infantile  affections,  as  measles,  and  in  the  absence  of 
other  symptoms,  especially  dyspnoea,  suggests  the  idea 
of  congenital  anomalies  of  the  heart  or  large  vessels. 
The  real  cause  of  cyanosis  in  congenital  cardiac  de- 
fects is  not  yet  sufficiently  clear.  When  the  two  ven- 
tricles communicate  with  each  other,  there  is  an  ad- 
mixture of  the  venous  blood  entering  the  right  ventricle 
with  the  arterial  blood  of  the  left,  and  the  same  con- 
dition results  if  the  aorta  and  pulmonary  artery  com- 
municate. Such  a  mixture  may  easily  become  venous 
in  the  peripheral  capillaries,  even  if  the  motor  power  of 
the  heart  and  the  rapidity  of  the  circulation  are  nor- 
mal. When  it  is  considered,  however,  that  serious 
defects  of  the  septum,  even  complete  absence  of  it,  does 
not  cause  cyanosis  during  the  first  years  of  life,  the  fact 
that  the  blood  becomes  abnormally  intermixed  should 
not  be  overestimated,  as  the  cause  of  cyanosis.  Much 
more  important  is  the  inefficiency  of  the  cardiac 
muscles,  especially  of  the  right  ventricle,  which  also 
interferes  with  the  supply  of  the  left  ventricle  and 
causes  the  circulation  in  the  capillaries  to  slacken. 


94         DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

STENOSIS  OF  THE  PULMONARY  ARTERY  AND 
INSUFFICIENCY  OF  THE  TRICUSPID 

The  congenital  cardiac  defects  which  are  accom- 
panied from  birth  by  cyanosis  and  disturbed  cardiac 
function  are  in  most  cases  comphcated  by  stenosis  of 
the  pulmonary  artery  and  insufficiency  of  the  tri- 
cuspid, so  that  the  cyanosis  is  explainable  by  simple 
stasis  of  the  venous  blood. 

OPEN  FORAMEN  OVALE 

At  autopsy,  an  open  foramen  ovale  is  frequently 
discovered,  and  yet  during  life  there  were  never 
any  indications  of  disturbed  circulation  in  the  cardiac 
cavities.  To  enable  the  blood  to  flow  over  from  the 
right  into  the  left  auricle,  the  pressure  in  the  right 
auricle  has  to  be  raised,  as  happens  in  tricuspid  in- 
sufficiency and  in  stenosis  of  the  tricuspid.  In  relative 
insufficiency,  or  in  dilatation  of  the  right  ventricle  with 
increased  pressure  in  the  right  auricle,  the  blood  may 
possibly  flow  over  from  the  right  into  the  left  auricle. 
This  may  happen  in  cardiac  insufficiency,  as  occurs 
in  emphysema  or  in  acute  affections  of  the  lungs. 
The  early  appearance  of  pronounced  cyanosis  in  one 
of  my  cases  of  pneumonia,  in  which  the  autopsy 
revealed  an  open  foramen  ovale,  may  perhaps  be 
explained  in  the  same  way.  I  also  recall  a  case  of 
t}^hoid,  where  a  loud  murmur  at  the  base  of  the  heart 
led  to  the  diagnosis  of  endocarditis,  which  Skoda,  a  few 
years  before,  but  unknown  to  me,  had  diagnosed  as  due 
to  an  open  foramen  ovale.     The  patient  recovered. 


DYSPNCEA   AND   CYANOSIS  95 

The  blood  may  flow  over  from  the  left  to  the  right 
auricle  when  there  is  an  associated  mitral  affection, 
and  thereby  lead  to  venous  engorgement  and  deep 
cyanosis  with  a  positive  venous  pulse. 

OPEN  DUCTUS  ARTERIOSUS 

The  phenomenon  of  an  open  ductus  arteriosus  nearly 
always  occurs  in  conjunction  with  other  anomalies  of 
the  heart,  as,  for  instance,  pulmonary  stenosis  and 
stenosis  of  the  aorta.  Some  show  cyanosis  with 
dyspnoea  and  intensified  heart-beat  from  birth,  and 
others  present  no  symptoms  whatever.  Even  combina- 
tions of  an  open  ductus  arteriosus  and  pulmonary 
stenosis  may  exist  for  years  without  giving  rise  to  any 
special  trouble,  even  cyanosis.  In  congenital,  uncom- 
plicated pulmonary  stenosis,  the  most  frequent  of  all 
congenital  affections,  cyanosis  may  either  be  absent  or 
slight,  and  show  temporary  exacerbations  under  the 
influence  of  psychic  excitement  and  intercurrent  affec- 
tions, or  after  severe  confinements.  Even  where  pul- 
monary tuberculosis  develops  in  a  case  of  pulmonary 
stenosis,  both  dyspnoea  and  cyanosis  may  be  absent  or 
present  only  to  a  limited  extent. 

STENOSIS  OF  THE  AORTA 

In  congenital  stenosis  of  the  aorta  cyanosis  occurs 
from  stasis  in  the  left  auricle,  and  the  right  ventricle. 
This  defective  development  not  infrequently  gives  rise 
to  attacks  of  suffocation. 

In  stenosis  of  the  isthmus  of  the  aorta  in  children. 


96        DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

cyanosis  and  dyspnoea  occur  with  laryngospasm  and 
congestion,  but  there  are  also  cases  without  these  mani- 
festations. Persons  suffering  from  stenosis  of  the 
isthmus  may  attain  quite  an  advanced  age  and  die  from 
the  usual  manifestations  of  cardiac  insufficiency  or 
sometimes  from  sudden  rupture  of  the  heart  or  aorta. 
A  case  observ^ed  by  me  showed  symptoms  of  angina 
pectoris  with  cyanotic  redness  of  the  face  during  the 
paroxysms.  In  congenital  stenosis  of  the  aorta  and 
arteries,  dyspnoea  and  cyanosis  develop  in  consequence 
of  secondary  changes  in  the  cardiac  muscle,  frequently 
caused  by  bodily  exertions,  excessive  indulgence  in  beer 
or  wine,  affections  of  the  valves  and  of  the  pericardium, 
or  by  infectious  diseases.  Affections  of  the  respira- 
tory system,  especially  an  acute  bronchial  catarrh,  may 
cause  considerable  dyspnoea. 

TRANSPOSITION  OF  THE  LARGE  VESSELS 

Contrary  to  the  defects  of  development  mentioned, 
nearly  all  cases  of  congenital  stenosis  and  insufficiency 
of  the  tricuspid  are  accompanied  by  cyanosis,  which  is 
explained  by  a  simple  engorgement  of  the  venous  blood 
in  precisely  the  same  way  as  is  the  affection  of  the  valve 
acquired  in  later  life.  Cyanosis,  too,  is  one  of  the 
most  constant  symptoms  in  the  transposition  of  the 
large  vessels.  Other  pathological  manifestations  like 
dyspnoea  and  attacks  of  suffocation,  which  occur  so 
frequently  in  pulmonary  stenosis  when  c}'anosis  in- 
creases, may  be  totally  absent  in  these  cases.  In  un- 
complicated cases    the  cardiac  sounds  are  pure  and 


DYSPNCEA   AND   CYANOSIS  97 

the  absence  of  cardiac  hypertrophy  is  diagnostically  im- 
portant. Cyanosis  in  the  transposition  of  arteries  may 
be  explained  not  only  by  engorgement,  but  also  by  the 
venous  condition  of  the  blood  circulating  in  the  sys- 
temic arteries.  The  tendency  to  spasms  associated 
with  errors  of  development  is  attributed  to  defective 
supply  of  the  brain  with  arterial  blood. 

MITRAL  STENOSIS    (CONGENITAL) 

A  special  group  in  the  symptomatology  is  composed 
of  those  forms  of  congenital,  strictly  mitral  stenosis,  to 
which  Duroziez  first  called  detailed  attention.  These 
are  the  special  forms  of  mitral  stenosis  in  which  the 
orifice  is  an  elastic  funnel,  and  the  edge  of  the  valve 
is  smooth  and  without  vegetations.  A  characteristic 
clinical  picture  corresponds  with  these  autopsy  findings 
of  a  purely  mitral  stenosis  without  vegetations  on  the 
valve.  It  is  a  striking  fact  that  no  etiology  can  be 
adduced  for  these  cardiac  defects,  as  the  anamnesis  re- 
veals no  articular  rheumatism,  scarlet  fever,  chorea  or 
angina.  It  appears,  however,  that  these  patients  in 
their  very  early  infancy  were  pale  and  weak,  and  that 
the  slightest  efforts  induced  paroxysms  of  palpitation 
and  dyspnoea.  One  or  the  other  predominated,  or, 
what  is  more  generally  the  case,  both  manifestations 
occurred  with  equal  intensity.  These  forms  of  mitral 
stenosis,  have  in  some,  a  small  left  ventricle  and  in 
others  both  ventricles  are  hypertrophied.  They  must 
be  regarded  as  congenital  defects  of  development  of  the 
mitral  orifice  with  hypoplasia  of  the  arteries,  as  the 


98         DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

functional  symptoms.  Especially  dyspnoea  and  palpi- 
tation often  date  from  earliest  infancy.  They  appear 
at  times  only  in  advanced  life,  but  in  girls  usually  be- 
tween the  fifteenth  and  twentieth  year.  These  young 
women  present  all  the  symptoms  of  chlorosis  and  com- 
plain particularly  about  palpitation  and  dyspnoea.  Aus- 
cultation reveals  the  sign  of  a  pure  mitral  stenosis, 
presystolic  murmur,  loud  first  sound,  accentuation  and 
frequently  reduplication  of  the  pulmonic  sound.  This 
type  is  described  as  chlorotic  mitral  stenosis.  At 
autopsy  there  is  found  pure  stenosis  of  the  mitral  with 
no  roughness  of  the  valve,  and  associated  with  a  thin, 
narrow,  elastic  aorta,  with  irregular  arteries,  and 
hypoplasia  of  the  internal  genitalia.  While  most  of 
these  cases  show  the  ordinary  symptom-complex  of 
chlorosis,  in  others  the  cardiac  conditions  displays  the 
more  prominent  signs:  dyspnoea,  stases,  cardiac  ar- 
rhythmia and  edema.  These  affections,  especially  dur- 
ing pregnancy,  may  lead  to  grave  difficulties  in 
breathing,  and  not  infrequently  to  rapid  death  from 
pulmonary  edema.  Some  cases  present  a  picture  which, 
on  account  of  the  emaciation,  pallor,  cough  and  ten- 
dency to  hemoptysis,  resembles  more  pulmonary  tuber- 
culosis than  a  cardiac  defect.  A  pregnant  woman 
brought  into  the  clinic  in  a  moribund  condition  exhib- 
ited numerous  rales  audible  over  both  lungs,  and  gave 
the  general  impression  of  phthisis.  The  pulmonary 
edema  subsided  and  auscultation  disclosed  the  presence 
of  a  pure  mitral  stenosis.  Etiology  of  any  kind  was 
not  obtainable,  but  the  anamnesis  showed  that  the  pa- 


DYSPNOEA   AND   CYANOSIS  99 

tient  as  a  child  was  always  pale  and  dyspnoeic,  and  at 
the  age  of  puberty  was  chlorotic  with  anomalies  of 
menstruation.  The  anamnesis,  together  with  the  ob- 
jective findings,  justified  the  diagnosis  of  a  congenital 
mitral  stenosis. 

From  these  explanations  about  the  congenital  cardiac 
defects,  it  follows  that  there  are  numerous  cases  of 
congenital  cyanosis  in  which  dyspnoea  and  cyanosis  do 
not  follow  a  parallel  course,  and  that  the  former  may 
sometimes  be  totally  absent.  Possibly  this  tolerance 
on  the  part  of  the  center  for  respiration  points  to  a 
reduced  requirement  for  oxygen  and  corresponds  with 
the  reduced  body  temperature,  apathy,  drowsiness  and 
the  other  signs  of  bodily  and  mental  inhibition  of  de- 
velopment so  often  observable  in  these  patients.  The 
respiratory  center,  having  lost  its  excitability,  does  not 
seem  to  react  well  to  the  poorly  oxygenated  blood  and 
to  the  dyspnoeic  irritations.  In  the  vast  majority  of 
cases,  however,  there  is  side  by  side  with  pronounced 
cyanosis  also  dyspnoea,  which,  from  slight  causes,  may 
become  intensified  to  the  point  of  suffocation,  and  is 
often  associated  with  palpitation  of  the  heart,  oppres- 
sion, fainting  and  other  signs  of  cardiac  weakness. 


II 

DYSPNCEA   AND   CYANOSIS    IN   ACQUIRED 
CARDIAC  LESIONS 

MITRAL  INSUFFICIENCY  AND  STENOSIS 

In  acquired  mitral  insufficiency  of  varied  but  mainly 
rheumatic  origin,  also  in  mitral  stenosis,  dyspnoea  is  a 
frequent  occurrence,  especially  in  the  stage  of  broken 
compensation  on  account  of  the  congested  lungs.  It 
is  characterized  by  rales  with  their  greatest  intensity  at 
the  base.  The  dyspnoea  may  attain  the  intensity  of 
orthopnoea.  An  upright  position  is  advised  to  diminish 
the  congestion  of  the  brain  and  to  aid  the  circulation 
of  the  oblongata.  Insomnia  in  these  patients  is  also 
explained  by  the  mechanical  congestion  of  the  brain. 

AORTIC  LESIONS 

In  contradistinction  to  affections  of  the  mitral  valve 
in  which  cyanosis  is  an  early  or  late  symptom  due  to 
venous  engorgement,  diseases  of  the  aortic  valve  are 
usually  distinguished  by  the  absence  of  cyanosis,  so 
that  there  is  a  certain  justification  for  speaking  of  a 
blue  facies  mitralis  and  a  pale  facies  aortica.  The 
mechanism  of  the  dyspnoea  in  aortic  conditions  is  also 
different.  In  affections  of  the  mitral  valve,  there  is, 
beside  the  congestion  of  the  lungs,  also  a  stasis  in  the 
oblongata  w^hich  increases  upon  lying  down,  owing  to 
the  retarded  flow  of  blood,  and  compels  patients  to 

lOO 


DYSPNCEA   AND    CYANOSIS  lOI 

select  a  more  upright  posture  in  bed.  In  insufficiency 
of  the  aortic  valve,  however,  the  important  dyspnoeic 
factor  is  the  ischemia  of  the  oblongata.  There  is,  as 
it  were,  the  pulsus  celer  which  poorly  nourishes  the 
center  of  respiration.  In  some  cases  the  periaortic 
processes  and  the  irritation  they  exert  upon  the 
branches  of  the  vagus  have  a  certain  importance  in 
the  causation  of  the  asthmatic  attacks.  This  also  ex- 
plains why  in  the  dyspnoea  and  cyanosis  of  mitral  affec- 
tions, digitalis  is  an  especially  successful  remedy,  while 
in  the  dyspncea  of  aortic  insufficiency  sedative  remedies 
like  potassium  bromide  and  opium  preparations  are 
more  effective.  Cyanosis,  however,  occurs  also  in  in- 
sufficiency of  the  aortic  valve,  if  there  are  complicating 
affections  of  the  mitral  or  if  bulging  of  the  interven- 
tricular septum  due  to  marked  excentric  hypertrophy 
of  the  left  ventricle  restricts  the  space  of  the  right  ven- 
tricle, which  in  its  turn  becomes  hypertrophied.  If 
fatty  degeneration  of  the  myocardium  makes  the 
left  ventricle  inefficient,  or  if  complicating  affections  of 
the  respiratory  system  and  of  the  serous  membranes 
as  pericarditis  develop.  In  aortic  stenosis,  therefore, 
unless  it  attains  a  high  degree  and  becomes  complicated, 
neither  dyspnoea  nor  cyanosis  is  present  in  the  path- 
ological picture. 

AFFECTIONS  OF  THE  PULMONARY  VALVE 

Cyanosis  is  not  a  constant  symptom  in  affections  of 
the  semilunar  valve  of  the  pulmonary  artery.  In  ac- 
quired insufficiency  of  the  pulmonary  valve  without 


102      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

stenosis,  which  rarely  occurs  from  rheumatic  endo- 
carditis, and  somewhat  more  often  from  trauma,  like 
a  blow  on  the  chest,  cyanosis  appears  in  the  beginning 
of  the  disease,  less  prominently  than  dyspnoea,  even  if 
the  patient  remains  absolutely  quiet.  In  the  further 
course,  cyanosis  follows  insufficiency  of  the  right  ven- 
tricle, as  in  other  cardiac  defects,  or  more  frequently 
embolism  of  the  pulmonary  artery.  In  acquired 
stenosis  of  the  pulmonary  artery  cyanosis  may  be  com- 
pletely absent  or  makes  its  appearance  at  an  advanced 
stage  of  the  affection.  The  dyspnoea  is  slight  even 
after  bodily  exertion  as  compared  with  the  frequency 
of  hemoptysis.  The  explanation  is  that  the  manifes- 
tations are  caused  less  by  the  valvular  defects  than  by 
the  frequent  combination  with  tuberculosis. 

ACUTE  ULCERATIVE  ENDOCARDITIS 

In  acute  ulcerative  endocarditis,  dyspnoea  and 
cyanosis  depend  less  on  the  primary  affection  than  on 
its  many  complications,  as  valvular  aneurisms,  cardiac 
aneurisms,  thrombosis.  They  are  also  affected  by  the 
localization  of  the  lesion  at  the  various  valves  and  their 
orifices,  on  the  degree  of  cardiac  inefficiency  and  the 
rapidity  of  its  development,  on  the  simultaneous  in- 
volvement of  the  myocardium  and  pericardium,  and 
finally  on  the  site  of  the  metastases  especially  of  mul- 
tiple emboli  of  the  lung  in  affections  of  the  right  heart. 
The  bacterial  endocarditis  which  occurs  in  the  course 
of  chronic  pulmonary  tuberculosis  has  a  special  tend- 
ency to  dyspnoea  and  hemoptysis.     As  a  rule  dyspnoea 


DYSPNCEA   AND    CYANOSIS  IO3 

is  but  slightly  pronounced  in  pure  endocarditis,  and  is 
in  many  cases  experienced  only  as  an  oppression  of  the 
chest,  which  may  increase  through  psychic  excitement 
and  by  sitting  up  in  bed.  The  occurrence  of  intense 
dyspnoea  therefore  requires  careful  examination,  espe- 
cially of  the  organs  of  respiration.  Cyanosis,  like 
dyspnoea,  plays  a  small  part  in  the  clinical  picture  of 
endocarditis.  Septic  forms  of  malignant  endocarditis 
may  show  pronounced  anemia  from  the  onset,  and  may 
be  mistaken  for  pernicious  anemia  (febris  pallida.) 

PURULENT  AORTITIS 

In  the  acute  forms  of  purulent  aortitis,  where  the 
abscess  perforates  the  intima  of  the  aorta  and  empties 
into  the  circulation,  retrosternal  pains,  girdle  sensation 
around  the  thorax,  pulsation  of  the  distended  aorta 
and  especially  paroxysmal  dyspnoea  with  prolonged  in- 
spiration, and  relatively  slight  difficulty  in  expiration, 
may  be  observed.  Intense  dyspnoea  and  cyanosis  with 
fear  of  death  may  occur  in  endocarditis  affecting  the 
aortic  valves  if  the  vegetations  on  the  valves  occlude 
the  aortic  orifice.  In  two  cases  of  pneumonia  under 
my  observation,  in  which  insufficiency  of  the  aortic 
valve  developed,  the  pulse  became  slower,  smaller  and 
harder,  and  a  systolic  murmur,  heard  over  the  aorta,  in 
addition  to  the  diastolic  one,  grew  continually  more 
protracted  and  distinct,  a  sign  of  progressively  develop- 
ing stenosis.  The  rapidity  of  the  pulse  disappeared,  it 
became  continually  smaller,  and  suddenly,  with  violent 
manifestations  of  asphyxia  and  general  epileptiform 


104      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

convulsions,  the  patients  died  from  occlusion  of  the 
aortic  orifice. 

PERICARDITIS   AND   ADHESIVE   PERICARDITIS 

In  pericarditis,  dyspnoea  and  cyanosis  are  inconstant 
phenomena.  Dyspncea  may  be  absent,  slight,  or  in- 
creased to  a  most  intense  degree,  orthopnoea,  with  the 
sensation  of  suffocation.  This  depends,  above  all, 
upon  the  quantity  of  the  exudate,  the  rapidity  of  its 
formation,  the  condition  of  the  m^-ocardium  as  well  as 
upon  complications  of  the  lung  and  pleura,  and  partly, 
also,  on  the  primary  affection,  which  caused  the  peri- 
carditis. In  large  exudates  it  is  caused  by  mechanical 
obstruction  to  the  flow  of  blood  into  the  auricles  and 
consequent  defective  filling  of  the  ventricles.  To  this 
is  added  the  direct  compression  of  the  vascular  trunks 
especially  of  the  superior  vena  cava,  the  more  so  if  the 
pericardium  is  distended  by  a  rapidly  developing  eflfu- 
sion.  Just  as  in  extensive  pleural  exudates,  dyspnoea 
may  be  slight  as  long  as  the  patient  remains  quiet  in 
one  position,  so  at  times  marked  exudates  into  the 
pericardium  do  not  cause  any  material  difficulty  in 
breathing.  There  is  often  a  disproportion  between  the 
intensity  of  the  dyspnoea  and  the  quantity  of  exudate  in 
tuberculous  pericarditis.  As  the  tuberculosis  spreads 
from  the  neighboring  organs — pleura,  lungs,  peritoneal 
and  mediastinal  glands — the  dyspnoea  may  also  ema- 
nate from  an  affection  of  these  structures.  Pericarditis 
in  the  course  of  miliar}'  tuberculosis  or  tuberculosis  of 
the  serous  membranes  sometimes  does  not  show  any 
material    increase    in    dyspnoea.     In    some    cases    of 


DYSPNCEA   AND   CYANOSIS  IO5' 

isolated  tuberculosis  of  the  pericardium,  dyspnoea  may, 
however,  attain  an  excessive  degree.  This  holds  good 
for  those  forms  of  pericarditis  which  sometimes  occur 
after  slight  pneumonia,  and  are  frequently  overlooked. 
The  appearance  of  dyspnoea  with  cyanosis  in  these  cases 
should  direct  attention  at  once  to  the  pericardium. 

Dyspnoea  in  pericarditis  may,  therefore,  be  due  to 
various  causes.  In  some  cases,  the  pains  from  in- 
volvement of  the  neighboring  pleura  may  cause 
dyspnoea;  perhaps  the  irritation  of  the  vagus  plays  a 
role,  in  others  it  may  be  an  affection  of  the  phrenic 
nerve.  Where  there  is  considerable  exudate,  the  pres- 
sure on  the  auricle  and  pulmonary  veins,  as  well  as 
on  the  left  lung,  may  cause  immobilization  of  the 
diaphragm  by  paralysis  or  downward  displacement. 
Very  large  exudates  may  restrict  the  thoracic  space  for 
all  structures.  Increase  of  dyspnoea  in  the  dorsal  posi- 
tion and  on  the  left  side  compels  patients  instantly  to 
assume  an  upright  posture  or  to  bend  forward,  and  to 
the  left,  in  order  to  relieve  the  pressure  on  the  organs 
lying  posterior,  especially  the  vena  cava  superior  and 
the  right  auricle,  and  possible  also  the  left  bronchus. 
This  certainly  presupposes  a  certain  mobility  of  the 
exudate,  which,  in  pericardial  exudates  with  partial 
adhesions,  is  not  always  present. 

Adhesions  of  the  heart  to  the  pericardium,  which 
frequently  exist  without  causing  any  symptoms,  are 
accompanied  by  dyspnoea  when  involvement  of  the 
muscular  substance  follows  inefficiency  of  the  left  ven- 
tricle, and  by  cyanosis,  with  manifestations  of  conges- 


I06      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

tion  and  dropsy  often  of  extreme  degree,  if  the  right 
ventricle  is  prominently  involved,  as  in  tricuspid  insuf- 
ficiency. 

In  consequence  of  the  compression  of  the  auricles 
and  the  venae  cavse,  and  also  from  cardiac  inefficiency 
through  involvement  of  the  myocardium  in  the  inflam- 
matory process,  we  find  associated  with  the  greatest 
accumulation  of  fluid  in  the  pericardium,  deep  cyanosis, 
edema  of  the  liver  and  lower  extremities,  pulse  hardly 
perceptible  and  paroxysms  of  extreme  dyspnoea.  In 
the  subacute  or  chronic  pericardial  exudates  of  anemic 
(tuberculous)  subjects,  the  exudate  is  generally  hemor- 
rhagic, and  the  cyanosis  in  spite  of  considerable 
dyspncea  and  orthopnoea  stands  either  quite  in  the  back- 
ground or  is  only  indicated  by  a  livid  coloration  of  the 
lips  and  mucous  membranes.  In  these  pericardial  ef- 
fusions, however,  which  are  a  part  manifestation  of 
miliary  tuberculosis,  cyanosis  usually  shows  a  consid- 
erable increase  in  intensity.  In  the  acute  exanthemata, 
especially  variola  and  scarlet  fever,  cyanosis  with  a 
greatly  accelerated  pulse  should  direct  attention  to  an 
existent  pericarditis.  The  same  holds  good  for  peri- 
carditis occurring  in  the  course  of  pneumonia,  especi- 
ally in  alcoholics ;  also  for  those  forms  of  pericarditis 
which  develop  in  the  course  of  chronic  affections,  as 
Bright's  disease,  scorbutus  and  carcinoma. 

HYDRO-,   HEM0-,  AND  PNEUMOPERICARDIUM 

In  hydropericardium,  dyspnoea  and  cyanosis  partly 
depend  upon  the  primary  affection,  like  Bright's  dis- 


DYSPNCEA   AND   CYANOSIS  IO7 

ease  and  cardiac  defects.  Large  accumulations  of 
fluid  are  able  to  produce  cyanosis  and  dyspnoea  by  com- 
pression of  the  lungs  and  auricles  as  in  pericarditis,  or 
to  augment  what  already  exists.  Dropsical  transu- 
dates into  the  pericardium,  in  contrast  to  pericardial 
exudates,  are  always  changing  and  the  congestion  is 
correspondingly  dependent,  increasing  or  decreasing 
with  each  change  of  position,  upon  the  stronger  or 
weaker  compression  of  the  auricles,  and  these  changes 
will  influence  the  appearance  and  intensity  of  the 
dyspnoea  and  cyanosis.  These  symptoms  varying  in 
the  upright  and  dorsal  positions,  may  direct  attention 
to  the  existence  of  an  hydropericardium  and  demand 
the  examination  of  the  cardiac  dullness  and  cardiac 
impulse  with  the  body  bent  forward.  This  may  also 
be  important  in  simultaneous  emphysema,  the  presence 
of  which  makes  the  diagnosis  of  hydropericardium 
diflicult. 

Effusions  of  blood  Into  the  pericardial  sac  (hemo- 
pericardium)  due  to  rupture  of  aneurisms  of  the 
aorta,  heart  or  coronary  arteries,  tearing  of  the  myo- 
cardium at  fatty  and  necrosed  places,  trauma  from 
without  or  swallowing  pointed  objects,  also  in  rare 
cases  to  perforation  of  tuberculous  glands,  lead  to 
death  with  dyspnoea,  pains  in  the  cardiac  region,  faint- 
ing, anemia  and  convulsions.  If  the  course  is  pro- 
tracted owing  to  the  small  size  of  the  tear  through 
which  the  blood  oozes  out  slowly  into  the  pericardium, 
cyanosis  or  livid  coloration,  generally  with  increasing 
enlargement  of  the  cardiac  dullness,  disappearance  of 


I08      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

the  cardiac  impulse  and  of  cardiac  sounds  in  conse- 
quence of  the  accumulation  of  blood  in  the  pericardial 
sac,  are  of  importance  for  the  diagnosis. 

Pneumopericardium  occurs  through  injuries  with 
pointed  objects,  either  from  without  by  stabbing  or 
from  within  by  swallowing  pointed  foreign  bodies,  by 
perforation  of  tuberculous  cavities  or  in  perforating 
pyo-pneumothorax ;  less  often  in  ulcerating  carcinoma 
of  the  esophagus  and  in  ulceration  of  the  stomach  into 
the  pericardium.  In  this  condition  dyspnoea,  sensation 
of  oppression  in  the  cardiac  region,  also  cyanosis  in 
consequence  of  the  compression  of  the  heart  and  lungs, 
are  constant  manifestations.  The  characteristic  phe- 
nomena of  auscultation  and  percussion  and  their  vari- 
ation, as  the  patient  changes  his  position,  make  the 
diagnosis  safe. 

FATTY  AND  MUSCULAR  DEGENERATIONS 

Dyspnoea  is  a  frequent  symptom  of  fatty  heart,  as 
in  valvular  lesions,  indicating  defective  motor  power 
of  the  heart  and  inefficiency  of  the  left  ventricle.  This 
dyspnoea  may  at  times  increase  after  bodily  exertion. 
The  pulse  frequency  is  considerably  accelerated  and 
there  may  be  orthopnoea  with  cyanosis  and  a  sensation 
of  fear  and  oppression. 

Also  other  affections  of  the  muscular  substance  of 
the  heart,  partly  primary'  and  in  part  secondary  to  in- 
terstitial or  parenchymatous  inflammations  after  in- 
fectious diseases,  weaken  the  cardiac  power  and  thus 
occasion   dyspnoea   and   cyanosis.     There   are   a    few 


DYSPNCEA  AND   CYANOSIS  IO9 

infectious  diseases  especially  which  are  associated  with 
the  signs  of  an  acute  or  chronic  affection  of  the  heart, 
both  during  their  febrile  course  and  in  convalescence. 
In  this  manner  dyspnoea  and  cyanosis  develop  in  the 
course  of  an  acute  articular  rheumatism,  not  only  in 
the  hyperpyretic  form,  but  also  in  cases  with  low  tem- 
perature, in  whom,  however,  cerebral  symptoms  and 
delirium  occur  during  the  first  few  days.  Salicylic 
preparations  are  administered  without  effect,  cardiac 
dullness  increases  and  the  pulse  becomes  small  and 
irregular.  Autopsy  in  these  cases  reveals  the  valves 
intact,  the  cardiac  cavities  much  distended  and  the 
muscle  excessively  friable.  Also  in  diphtheria  there 
are  similar  degenerations  of  the  cardiac  muscle  and 
of  the  coronary  vessels,  both  during  and  after  the  acute 
stage,  and  they  are  not  infrequently  the  cause  of  sud- 
den death.  The  same  is  true  in  scarlet  fever,  dysen- 
tery, and  typhus  fever.  So  far  as  the  latter  is 
concerned,  dyspncea  and  cyanosis  occur  even  during 
convalescence  from  insignificant  causes,  and  this  is  a 
sign  of  the  involvement  of  the  heart  and  arteries.  The 
changes  of  the  myocardium  and  of  the  vessels  in  en- 
teric fever  are  recognized  both  during  the  course  of 
the  disease  and  in  convalescence  by  various  clinical 
signs  of  cardiac  weakness,  as  cyanosis,  puffy  face, 
edema  of  the  ankles,  weakness  of  the  first  mitral 
sound,  arrhythmia  with  low  blood  pressure,  slight 
diuresis  and  not  infrequently  albuminuria.  These  mani- 
festations may  sometimes  lead  to  early  and  even 
sudden  death,  but  on  the  other  hand  they  may  pass  off 


no      DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

quickly  and  without  any  evil  consequences.  The  oc- 
currence of  the  embryonic  heart  rhythm  with  cyanosis 
of  the  face  and  extremities,  diminution  of  diuresis, 
lowering-  of  the  skin  temperature  with  elevation  of  the 
body  temperature  are,  as  a  rule,  preagonal  symptoms. 
Cyanosis  is  also  observed  in  rare  affections  of  the 
heart:  amyloid  degeneration,  cardiac  abscess,  also  in 
cardiac  tumors:  carcinoma,  sarcoma,  tubercles,  syphi- 
loma, actinomycosis;  and  in  parasitic  affections  like 
cysticerci  and  echinococci. 

THROMBOSIS   OF  THE   HEART 

Intense  dyspnoea,  frequently  accompanied  by  bloody 
expectoration,  and  rapidly  increasing  cyanosis  with 
coldness  of  the  extremities  is  observed  in  thrombosis 
of  the  heart.  Thrombi  situated  in  the  left  auricle  and 
causing  stenosis  of  the  mitral  orifice,  or  right-sided 
cardiac  thrombi  migrating  into  the  pulmonary  artery, 
will,  as  a  matter  of  course,  be  associated  with  dyspnoea 
and  cyanosis.  In  extensive  thrombi  of  the  left  auricle 
pressure  from  without  may  diminish  the  lumen  of  the 
pulmonary  artery,  in  thrombi  of  the  right  auricle  that 
of  the  aorta,  and  both  give  rise  to  systolic  stenotic 
murmurs  and  deficient  filling  of  the  corresponding 
vascular  systems.  While  many  cases  exhibit  consider- 
able dyspnoea  and  cyanosis,  there  are  on  the  contrary 
cases  of  cardiac  thrombosis  without  cyanosis  and  with- 
out material  dyspnoea,  in  which  manifestations  of  de- 
fective filling  of  the  arterial  system  are  evident;  as 
a  very  frequent,  small,  irregular,  radial  pulse,  great 
pallor,  sensation  of  fear  and  fainting  attacks.    In  other 


DYSPNCEA   AND   CYANOSIS  III 

cases,  symptoms  arising  from  distant  organs  dominate 
the  clinical  picture.  In  a  patient  under  my  observation 
with  carcinoma  of  the  stomach,  thrombosis  of  the  left 
heart  occurred  at  an  atheromatous  mitral  valve  and 
gave  on  auscultation  the  signs  of  mitral  insufficiency, 
which  led  to  a  fatal  embolus  in  the  artery  of  the  fossa 
of  Sylvius.  Manifestations  on  the  part  of  the  stomach 
and  intestine,  as  emboli  of  the  intestinal  arteries,  ap- 
pear in  other  cases.  Nevertheless,  in  the  majority  of 
cases  cardiac  manifestations  are  pronounced.  In  our 
clinic  a  waiter,  twenty-seven  years  of  age,  suffered 
from  dilatation  of  the  heart,  in  the  stage  of  ruptured 
compensation,  ascites  and  anasarca.  Patient  died 
within  a  few  days,  after  increasing  dyspnoea  and  cya- 
nosis, palpitation,  gallop  rhythm,  reduction  of  blood 
pressure  and  reduplication  of  the  second  pulmonic 
sound.  The  autopsy  showed  atheroma  of  the  coronary 
vessels  with  the  formation  of  extensive  cardiac  in- 
durations in  the  area  of  the  left  ventricle  (aneurisma 
partiale  cordis)  and  correspondingly  distended  parie- 
tal thrombosis. 

THEORIES   OF    CARDIAC    DYSPNCEA    (bASCH's   AND 

fraenkel's) 
According  to  Basch,  cardiac  dyspnoea  occurs  in  the 
first  place  from  enlargement  in  the  volume  of  the  lung, 
associated  with  congestion  which  he  designates  as  pul- 
monary rigidity  (Lungenstarrheit).  Owing  to  the 
inefficiency  of  the  left  ventricle  and  the  correspond- 
ingly greater  activity  thrown  upon  the  right  ventricle, 
the  lung  becomes  rigid,  distends  only  with  difficulty; 


112       DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

and  thus  forms  an  impediment  to  respiration.  Car- 
diac dyspnoea  owes  its  origin  to  this  mechanical 
obstruction,  not  to  a  neurotic  origin  occasioned  by  the 
chemical  properties  of  the  blood. 

A.  Fraenkel  attaches  great  importance  to  the  en- 
gorgement of  the  bronchial  mucous  membrane  in  the 
development  of  cardiac  dyspnoea  and  considers  the 
participation  of  a  secondary  bronchospasm  not  entirely 
excluded  as  a  factor  in  the  paroxysms  of  cardiac 
asthma.  Fraenkel's  theory  explains  more  simply  the 
suddenly  appearing  resistance  to  the  circulation  than 
does  Basch's  pulmonary  rigidity,  although  the  latter's 
experimental  investigations  and  explanatory  state- 
ments concerning  the  conditions  of  blood  pressure  and 
circulation  in  cardiac  asthma  are  of  fundamental  im- 
portance for  the  understanding  of  many  phenomena 
occurring  in  connection  therewith. 

Basch's  doctrine  of  secondary  inefficiency  of  the 
left  ventricle  as  a  sequel  to  increased  intracardiac  pres- 
sure which  originates  under  the  influence  of  high 
arterial  pressure,  explains  why  the  gravest  paroxysms 
of  cardiac  dyspnoea  may  occur  not  only  with  low  blood 
pressure  as  in  mitral  stenosis,  but  also  with  normal  or 
even  increased  arterial  pressure.  The  left  ventricle, 
as  it  were,  becomes  tired  in  the  struggle  with  the  in- 
creased powers  of  resistance  on  the  part  of  the  arteries, 
and  the  consequence  of  such  secondary  inefficiency  of 
the  heart  is  increased  pressure  in  the  left  auricle  and 
the  pulmonary  capillaries. 

The  inefficiency  of  the  left  ventricle  occurs  more 


DYSPNOEA   AND   CYANOSIS  II3 

readily  if  the  heart  is  already  in  a  badly  nourished 
state  and  if  the  demand  made  upon  Its  power  is  great. 
This  kind  of  dyspnoea,  occurring  as  it  does  if  the  left 
ventricle  has  to  overcome  considerable  obstruction, 
happens  very  frequently  in  arteriosclerosis  and  in  con- 
traction of  the  kidneys. 

FINAL  CAUSE  OF  CARDIAC  DYSPNCEA 

Since  the  final  cause  of  dyspnoea  in  affections  of  the 
heart  is  inefficiency  of  the  left  ventricle,  and  is  due  to 
the  fact  that  the  latter  does  not  completely  empty  its 
contents  into  the  arteries  and  thus  causes  engorge- 
ment of  blood  in  the  left  auricle  and  lungs,  the  pulse 
in  the  fully  developed  paroxysm  of  cardiac  asthma, 
although  perhaps  strong  enough  at  first,  becomes 
softer  and  smaller.  There  may,  however,  be  elevation 
of  the  blood  pressure  under  the  influence  of  the  blood 
in  dyspnoea,  exciting  the  vasomotor  centers.  The  in- 
creased tension  of  the  pulse  may  even  continue  during 
the  paroxysm  together  with  dyspnoea  and  especially 
cyanosis,  particularly  if  the  primary  affection  is  asso- 
ciated with  abnormally  high  blood  pressure. 

DYSPNOEA    AND    BLOOD    PRESSURE 

There  are  cases  in  which  the  dyspnoea  improves  un- 
der falling  blood  pressure,  and  also  others  in  which 
the  dyspnoea  decreases  although  the  blood  pressure 
rises.  The  latter  is,  for  instance,  the  case  after  the 
administration  of  digitalis  in  mitral  stenosis.  Digi- 
talis, as  a  rule,  has  the  effect  of  increasing  the  arterial 


114      DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

pressure.  The  causes  vary :  increase  of  cardiac  power, 
lengthening  of  the  systole  and  constriction  of  the  ves- 
sels. Occasionally,  however,  the  cardiac  function  im- 
proves under  digitalis  in  both  systole  and  diastole, 
while  the  pathologically  increased  blood  pressure 
diminishes.  In  our  clinic  there  have  been  several  cases 
with  high  blood  pressure,  dyspnoea  and  cyanosis,  in 
which  the  blood  pressure  after  the  administration  of 
digitalis  fell,  the  dyspnoea  and  cyanosis  subsided,  while 
the  other  phenomena  of  stasis,  such  as  albuminuria, 
remained  practically  stationary.  Here  it  must  be  as- 
sumed that  in  consequence  of  the  better  contraction  of 
the  left  ventricle  and  the  strengthening  of  the  right 
ventricle  of  the  heart,  the  carbon  dioxid  tension 
was  decreased  by  the  improved  arterialization  of  the 
pulmonary  and  coronary  blood,  thereby  lowering  the 
excitation  of  the  center  of  respiration.  This  is  the 
condition  in  arteriosclerosis,  where  there  is  cyanosis 
with  high  blood  pressure:  the  state  which  Sahli  de- 
scribes as  high-pressure  congestion.  Traube  pointed 
out  that  digitalis,  administered  in  such  cases  in  order 
to  mitigate  the  symptoms,  may  expose  the  patient  to 
the  danger  of  cerebral  hemorrhage.  These  apprehen- 
sions are  certainly  justified  when  it  is  considered  that 
generally  digitalis  increases  the  arterial  pressure  and 
that  a  possible  increase  of  pressure  throws  an  addi- 
tional task  upon  an  already  inefficient  heart.  Sahli, 
on  the  other  hand,  made  the  important  statement  at 
the  Nineteenth  Congress  for  Internal  Medicine  in  Ber- 
lin, 190 1,  that  digitalis  was  capable  not  only  of  re- 


DYSPNCEA   AND   CYANOSIS  II5 

moving  the  engorgement  in  high  pressure  congestion, 
but  also  of  considerably  reducing  the  high  blood  pres- 
sure, instead  of  further  increasing  it.  This  paradoxi- 
cal result  of  digitalis  was  partly  explained  by  Sahli's 
statement  that  there  was  a  lessening  of  the  vascular 
spasm  by  removal  of  the  dyspnoea,  and  partly  by  the 
assumption  that  the  enlarged  digitalis  pulse  was  capa- 
ble of  overcoming  the  peripheral  obstruction  in  the 
finest  arteries,  thus  dilating  the  vessels.  Based  upon 
these  experiences,  Sahli  has  pronounced  the  dictum 
that  high  arterial  pressure  in  itself  is  no  contra-indica- 
tion  to  the  administration  of  digitalis.  Our  own  ex- 
perience entirely  agrees  with  that  of  Sahli  in  this 
respect,  for  we,  too,  have  had  cases  of  arteriosclerosis 
with  dyspnoea,  considerable  cyanosis  and  increased 
blood  pressure,  in  which  the  latter  sank,  dyspnoea  de- 
creased and  cyanosis  disappeared  after  the  administra- 
tion of  digitalis. 


Ill 

DYSPNOEA  AND   CYANOSIS   IN   VASCULAR 
LESIONS 

ARTERIOSCLEROSIS  AND  ANEMIA 

Those  cases  of  arteriosclerosis  act  very  differently 
where,  although  dyspnoea  is  associated  with  high  blood 
pressure,  there  is  anemia  Instead  of  cyanosis.  If  these 
cases  are  complicated  with  aortic  insufficiency,  there 
occurs  consequent  upon  the  dilatation  of  the  abdominal 
vessels  an  aspiration  of  the  blood,  as  it  were,  into  the 
latter.  These  patients  bleed  into  themselves.  There 
Is  an  actual  abdominal  plethora  in  consequence  of  in- 
travascular bleeding,  while  the  skin  and  brain  may 
perhaps  be  anemic  in  consequence  of  secondary  vaso- 
constriction. The  patients  are  as  pale  as  if  In  a  faint 
and  yet  they  have  not  lost  a  drop  of  blood,  and  every 
drop  is  normal. 

ARTERIOSCLEROSIS    AND    PSEUDO-ANEMIA 

These  forms  of  chronic  pseudo-anemia  In  arterio- 
sclerosis arise  from  unequal  distribution  of  blood, 
shown  by  hyperemia  of  the  abdominal  vessels  and 
complemental  anemia  of  the  skin  and  are  possibly 
caused  by  dilatation  of  the  intestinal  vessels,  conse- 
quent upon  Irritation  of  the  depressor  fibers  of  the 

Ii6 


DYSPNCEA  AND   CYANOSIS  II7 

vagus.  Paralysis  of  the  vasomotors  of  the  splanchnic 
nerve  may  also  have  the  same  effect.  To  this  group 
very  likely  belong  those  cases  which  are  observed  be- 
fore the  deposit  of  inflammatory  exudates  in  the  peri- 
toneum, as  in  polyserositis,  perihepatitis  and  peritonitis 
associated  with  affections  of  the  heart.  Nevertheless, 
in  these  pale  arteriosclerotic  patients  there  may  be  high 
blood  pressure  In  consequence  of  partial  vasoconstric- 
tion. If  in  these  cases  digitalis  is  administered  on 
account  of  dyspnoea,  our  experience  shows  that,  in 
contrast  to  the  cyanotic  forms,  the  blood  pressure  rises 
and  the  dyspnoea  increases.  The  same  result  is  ex- 
perienced in  aortic  insufficiency,  with  excessive  pallor 
of  the  skin  and  signs  of  engorgement  of  the  abdominal 
organs.  These  pale  cases  of  aortic  Insufficiency  are 
therefore  not  suitable  for  digitalis  treatment.  Their 
dyspnoea  would  be  intensified  with  increasing  blood 
pressure,  while  by  way  of  contrast,  the  blue  cases  of 
aortic  insufficiency,  in  which  dyspnoea  Is  associated 
with  cyanosis,  occasionally  react  to  digitalis  with  bene- 
ficial results, 

ARTERIOSCLEROSIS   AND  THE   HEART 

In  the  vast  majority  of  cases  dyspnoea  In  arterio- 
sclerosis is  caused  by  temporary  or  permanent  ineffi- 
ciency of  the  left  ventricle,  while  the  dyspnoeilc 
paroxysms  are  associated  with  stasis  In  the  lungs,  pul- 
monary rales  and  sometimes  with  albuminous  expec- 
toration tinged  with  blood  as  In  cardiac  asthma.  On 
the  other  hand,  there  are  cases  in  which  there  is  a 


Il8      DISORDERS   OF  RESPIRATION   AND  CIRCULATION 

surprising  disproportion  betvreen  the  intensity  of  the 
dyspnoea  and  the  physical  manifestations  in  the  lungs. 
"  Dry  "  dyspnoea,  without  expectoration,  in  which  the 
vesicular  respiration  is  diminished,  with  only  very  few 
if  any  dry  rales,  recalls  in  a  way  bronchial  asthma, 
from  which,  however,  it  is  chiefly  distinguished  in  that 
inspiration  and  expiration  are  almost  uniformly  pro- 
longed. In  most  cases,  however,  there  is  a  combina- 
tion of  both  affections,  in  the  sense  of  a  composite  of 
cardiac  dyspncea  and  bronchial  spasm.  Possibly  some 
periaortic  processes,  involving  branches  of  the  pneu- 
mogastric  ner^^e  may  here  play  a  role.  This  must  at 
least  be  assumed  for  those  cases  of  asthma,  accom- 
panied by  stenocardiac  paroxysms  and  not  based  on 
coronary  sclerosis,  that  they  be  interpreted  as  angina 
plexus. 

This  enumeration  by  no  means  exhausts  the  causes 
of  dyspnoea  in  arteriosclerosis.  Its  appearance  is  in  the 
first  place  dependent  upon  the  question  whether  the 
heart,  which  compensates  for  the  diminished  perform- 
ance of  the  arteries,  is  hypertrophied,  and  how  long  it 
will  remain  capable  of  functionating  in  this  condition. 
The  sclerosis  of  the  arteries  may,  as  is  well  known,  be 
irregularly  disseminated.  It  has  often  been  obsen^ed 
that  considerable  change  in  the  arteries  of  one  organ 
are  not  always  accompanied  by  equally  important 
change  in  those  of  another.  Therefore,  the  occurrence 
and  the  polymorphism  in  the  varieties  of  dyspnoea  de- 
pend upon  the  localization  in  those  organs  whose  dis- 
turbances of  circulation  and  nutrition  react  upon  the 


dyspnceA  and  cyanosis  119 

condition  of  respiration  and  circulation.  In  regard  to 
localization  in  the  respiratory  apparatus,  the  intercostal 
and  bronchial  nutrient  arteries  should  be  considered, 
and  in  regard  to  arteriosclerosis  of  the  heart,  both 
coronary  arteries.  When  it  is  remembered  that  nu- 
merous branches  arise  from  the  descending  aorta;  the 
posterior  bronchial,  the  esophageal,  the  mediastinal 
and  especially  the  intercostal  arteries,  which  supply  both 
the  ribs  and  costal  muscles,  it  is  clear  that  an  extensive 
sclerosis  of  the  thoracic  aorta  with  constriction  at  the 
points  of  radiation  of  these  small  branches,  will  lead 
to  a  defective  blood  supply  of  the  corresponding 
regions.  Atheroma  of  the  aorta,  therefore,  may  lead 
to  disturbed  nutrition  of  the  bronchi,  lungs,  ribs  and 
muscles.  In  this  manner  secondary  emphysema  with 
atrophy  of  the  lungs  and  thorax,  may  result,  and  both 
this  condition  as  well  as  secondary  bronchial  catarrh 
may  have  to  be  taken  into  account  as  etiological  factors 
for  dyspnoea. 

The  significance  of  arteriosclerosis  for  the  heart  is 
evident  since  the  functional  activity  of  the  latter  de- 
pends upon  whether  the  coronary  arteries,  which 
nourish  the  heart,  remain  intact  or  are  involved  at  an 
early  period.  In  the  latter  case,  the  hypertrophy  of 
the  heart  is  checked  in  spite  of  increased  peripheral 
obstruction,  caused  by  the  sclerosis  of  the  trunk 
arteries,  and  there  results  a  general  degeneration  of  the 
myocardium  or  partial  myomalacia  with  its  sequelae, 
as  aneurism  of  the  heart  and  the  formation  of  indura- 
tions.    In  these  cases  a  clinically  well  characterized 


120      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

s;y-mptom-complex  may  dominate  the  pathological  pic- 
ture, i.  e.,  angina  pectoris  coronaria.  In  pure  cases  of 
coronary  angina  both  dyspnoea  and  cyanosis  are  absent. 
In  spite  of  the  oppression  of  the  chest,  respiration  is 
either  not  changed  at  all  or  only  slightly  deeper  or 
more  frequent.  Sometimes  there  is  even  apnoea,  when 
the  patient  immobilizes  the  thorax  in  consequence  of 
great  pain.  The  face  is  as  a  rule  pale  during  the  steno- 
cardial  attacks.  In  other  cases,  there  is  cyanosis  of 
the  lips  which  stands  out  in  striking  contrast  to  the 
pallor  of  the  skin.  There  are  also  combinations  of 
angina  pectoris  with  cardiac  asthma,  in  which  steno- 
cardial  symptoms  occur  with  dyspnoea.  If  the  course 
of  the  affection  becomes  protracted,  there  will  also  be 
intense  cyanosis  with  acute  emphysema,  congestion  of 
the  lungs  and  bloody  expectoration.  The  acute  exacer- 
bations of  chronic  aortitis  and  especially  of  periaortitis 
may,  likewise,  exercise  an  influence  upon  the  cardiac 
plexus  and  its  pulmonary  fibers  and  lead  to  death  from 
asphyxiation  through  acute  or  subacute  edema  of  the 
lungs,  under  manifestations  of  severe  dyspnoea  and 
cyanosis  with  aggravated  and  protracted  inspiration. 

Dyspnoea  resulting  from  localization  of  arterio- 
sclerosis in  the  circulatory  apparatus,  especially  in  the 
heart,  depends,  as  may  easily  be  understood,  on  ineffi- 
ciency of  the  left  ventricle,  with  increased  pressure  in 
the  left  auricle,  and  later  stasis  of  the  lungs.  In  these 
cases  the  blood  pressure  is  low,  unless  dyspnoea  and 
defective  arterialization  of  the  blood  cause  a  vascular 
spasm  by  increased  vasomotor  irritability  and  with  it 


DYSPNCEA   and   cyanosis  121 

an  augmentation  of  the  resistance.  This  form  of 
dyspnoea  is  accompanied  by  cyanosis,  and,  as  explained, 
the  increased  blood  pressure  is  a  prognostically  favor- 
able sign  if  the  dyspnoea  decreases  under  the  influence 
of  therapeutic  measures.  In  cases  where  inefficiency 
of  the  left  heart  is  developed  under  the  influence  of 
high  aortic  pressure,  there  will  be  dyspnoea  in  conse- 
quence of  the  increased  pressure  in  the  pulmonary  ves- 
sels, if  the  heart  is  unable  to  overcome  the  resistance. 
The  right  heart  is  compelled  to  empty  its  contents  into 
the  pulmonary  artery  with  great  force.  If  the  right 
ventricle  also  becomes  inefficient,  and  dilates,  there  may 
be  distention  of  the  valvular  ring,  and  the  tricuspid 
valve  becomes  incompetent.  The  insufficiency  of  this 
valve  is  equivalent,  to  a  certain  extent,  to  venesection 
of  the  pulmonary  artery  or  rather  of  the  pulmonary 
circulation.  This  causes  the  blood  pressure  in  the  pul- 
monary area  to  sink,  the  formerly  accentuated  second 
pulmonic  sound  becomes  weaker,  and  the  cardiac 
dyspnoea  frequently  diminishes,  while  cyanosis  with 
manifestations  of  congestion  increases  in  the  area  of 
the  vena  cava.  This  decrease  of  dyspnoea  by  the  open- 
ing of  the  safety  valve,  namely,  the  tricuspid  orifice, 
with  simultaneously  increasing  cyanosis,  does  not  last 
long,  because  the  cyanosis  of  the  brain,  medulla  ob- 
longata and  kidneys,  as  well  as  the  engorgement  of  the 
blood  in  the  coronary  veins,  produce  new  factors  for 
causing  dyspnoea  which  is  then  not  of  cardiac,  but 
rather  of  cardio-bulbar  or  cardio-renal  origin, 


122      DISORDERS   OF  RESPIRATION   AND   CIRCULATION 
ARTERIO-SCLEROSIS  AND  THE  KIDNEYS 

The  determination  of  the  localization  of  the  condi- 
tion in  the  kidneys  is  of  great  importance  among  the 
myriad  causes  of  dyspnoea  in  arteriosclerosis.  As  the 
arteriosclerotic  affection  develops  in  the  kidneys,  the 
latter  become  inefficient.  The  consequence  of  this  in- 
efficiency is  a  retention  of  toxic  metabolic  products 
which  are  able  to  exert  an  irritation  upon  the  oblon- 
gata, the  pulmonar}'  vessels,  and  perhaps  also  on  the 
bronchial  muscles.  The  accumulation  of  oxydizable 
metabolic  products  should  not  be  underrated,  as  they 
prey  upon  the  oxygen  and  lead  to  improverishment  of 
the  blood  and  tissues  in  oxygen.  These  factors  may 
produce  dyspnoea  (sine  materia)  in  the  sense  of  Char- 
cot, in  which  dyspncea  and  oppression  bear  no  rela- 
tion to  the  physical  signs  of  the  heart  and  lungs  or  to 
the  findings  at  autopsy.  This  form  of  dyspnoea  is  to 
be  traced  back  to  direct  irritation  of  the  respiratory 
center,  and  is  therefore  purely  toxic  and  of  bulbar  ori- 
gin, resem.bling  uremia  b}''  its  accompanying  manifes- 
tations, as  fibrillary  twitchings,  exaggeration  of  the 
tendon  reflexes,  formication  of  the  fingers  and  toes, 
vertigo,  tinnitus  aurium,  headache,  pol}Tjria,  etc.  The 
occurrence  of  albuminuria,  of  renal  elements  in  the 
urine  and  the  reaction  of  the  renal  affections  upon  the 
heart,  depend  above  all  upon  the  degree  of  injurv^  to 
the  renal  tissue.  It  should  not  be  overlooked,  how- 
ever, that  in  old  people  the  arteriosclerotic  affection  of 
the  kidneys,  w^here  they  are  no  pronounced  symptoms 
of  nephritic  disorder,  may  give  rise  to  dyspnoea  which 


DYSPNCEA   AND   CYANOSIS  I23 

is  sometimes  expressed  only  by  polypnoea  with  deep- 
ening and  acceleration  of  the  movements  of  respiration. 
Huchard  describes  a  special  form  of  toxic  alimentary 
dyspnoea  which  occurs  in  the  beginning  of  arterio- 
sclerosis. This  stage  is  called  the  presclerotic  and  is 
characterized  by  permanent  elevation  of  the  blood  pres- 
sure. In  these  forms  of  dyspnoea  there  are  functional 
disturbances  of  the  renal  secretion,  occasioned  by  spasm 
of  the  renal  vessels.  There  is  intermittent  dysphagia, 
an  intermittent  claudication,  such  as  also  occurs  in  other 
organs  in  consequence  of  deficient  circulation  and  con- 
striction of  the  vascular  lumen.  The  renal  inefficiency 
is  principally  exhibited  by  defective  excretion  of  toxins 
which  are  elaborated  from  the  food  and  which  produce 
paroxysms  of  dyspnoea,  especially  at  night.  The  cause 
of  their  occurrence  at  night  is  explained  according  to 
French  clinicians  by  the  accumulation  of  toxins  in  the 
blood  at  night.  This  is  based  on  the  investigations  of 
Bouchard,  who  determined  that  the  toxicity  of  urine 
excreted  at  night  is  diminished.  Importance  is  also  at- 
tributed to  the  effect  of  the  toxins  upon  the  vessels, 
which  leads  to  increase  of  the  blood  pressure.  The 
final  result  of  autointoxication,  therefore,  is  a  vascular 
spasm  and  the  mechanism  of  dyspnoea  is  the  same  as 
is  observed  in  the  increase  of  blood  pressure  from  other 
causes  due  to  increased  demands  upon  and  secondary 
inefficiency  of  the  left  ventricle.  Toxic  alimentary 
dyspnoea  deserves  special  interest,  because  it  can  be 
successfully  treated  by  withholding  meat  and  replacing 
it  by  a  lacto-vegetable  diet. 


124      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 
CEREBRAL    AND    SPINAL    ARTERIOSCLEROSIS 

In  contrast  to  the  bulbar  form  of  dyspnoea  of 
toxic  origin,  those  forms  should  be  mentioned  which 
result  from  the  localization  of  the  arteriosclerosis  in  the 
brain  and  medulla  oblongata.  These  are  disturbances 
of  respiration  which  accompany  Stokes-Adams  disease 
and  in  which  ischemia  of  the  oblongata  is  the  most 
important  factor  in  the  pathological  picture.  The 
Cheyne-Stokes'  respiratory  phenomenon,  which  is  so 
frequently  observed  in  the  cerebral  and  renal  localiza- 
tion of  arteriosclerosis,  also  belongs  to  this  group. 
Other  forms  of  paroxysmal  dyspnoea  which  occur  under 
the  picture  of  sudden,  sometimes  periodically  inter- 
mittent, asthmatic  attacks,  with  normal  function  of  the 
heart  and  kidneys  in  pale  arteriosclerotic  subjects,  and 
which  defy  all  therapy  with  the  exception  of  morphin, 
should  also  be  included.  Huchard  has  observed  such 
cases  and  considers  them  due  to  sclerosis  of  the  bulbar 
arteries. 

SIGNIFICANCE   OF  DYSPNOEA   IN   ARTERIOSCLEROSIS 

It  will  thus  be  seen  that  dyspnoea  in  arteriosclerosis 
may  be  produced  by  various  factors;  central  local  ir- 
ritation of  the  oblongata,  toxic  and  uremic  influences 
in  renal  insufficiency,  irritation  of  the  pneumogastric 
nen'-e  in  peri-aortic  affections,  secondary  emphysema 
and  bronchitis.  The  most  frequent  cause  of  dyspnoea 
is  inefficiency  of  the  heart,  the  contributing  factor  to 
which  may,  in  a  large  number  of  cases,  be  found  in  an 
increased  blood  pressure.     In  all  forms  of  dyspnoea 


DYSPNCEA   AND   CYANOSIS  12$ 

with  high  blood  pressure,  the  object  of  the  therapy  is 
to  reduce  it,  and  in  these  cases  decrease  in  the  dyspnoea 
corresponds  to  the  fall  in  the  blood  pressure.  All 
factors  which  raise  the  blood  pressure  may  disturb  the 
cardiac  equilibrium  and  produce  acute  paroxysms  of 
cardiac  asthma.  In  this  connection  a  case  mentioned 
by  Basch  is  interesting,  because,  after  the  adminis- 
tration of  atropin  to  correct  arrhythmia,  an  asthmatic 
paroxysm  occurred  with  tachycardia,  palpitation  and 
increase  of  the  blood  pressure. 

Not  evei-y  arteriosclerotic  patient  with  high  blood 
pressure  is  dyspnoeic.  There  are  individuals  with  very 
high  blood  pressure  who  do  not  for  years  exhibit  any 
dyspnoea  or  cardiac  weakness,  if  the  heart  remains 
efficient  and  accustoms  itself  to  the  increased  task. 
The  fall  of  the  blood  pressure  during  the  dyspnoea  of 
arteriosclerosis  may  have  different  meanings,  favorable 
and  unfavorable.  The  fall  is  unfavorable,  if,  owing  to 
diminished  cardiac  power,  the  left  ventricle  expels  too 
little  blood  into  the  aorta.  The  pressure  in  the  left 
auricle  and  pulmonary  vessels  rises,  while  dyspnoea  and 
cyanosis  increase.  But  there  are  cases  where  the  blood 
pressure  sinks  and  respiration  becomes  free,  but  the 
general  condition  nevertheless  is  worse.  That  happens 
when  complications  occur,  such  as  hemorrhages  or  sec- 
ondary anemia  with  quantitative  diminution  of  the 
blood,  splanchnic  engorgement  to  which  reference  has 
already  been  made,  ascites  and  dropsy,  in  subjects  with 
sclerosis  of  the  visceral  region,  due  to  a  diminished  vis 
a  tergo.     So  far  as  prognosis  is  concerned,  therefore. 


126      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

neither  the  abatement  of  the  dyspncea  nor  the  reduc- 
tion of  the  vascular  tension  can  always  be  interpreted 
as  an  improvement  of  the  cardiac  function. 

From  these  obser\'ations  on  dyspnoea  in  cardiac  de- 
fects and  arteriosclerosis,  it  follows  that  dyspnoea  may 
be  produced  from  various  causes  and  causative  factors, 
whether  it  is  dyspnoea  from  exertion  {Dypsnoe 
d' effort),  or  paroxysmal  dyspnoea,  associated  with 
oppression  and  fear,  the  true  cardiac  asthma.  In  order 
to  form  a  judgment  on  the  nature  and  causes  of 
dyspnoeic  paroxysms  in  a  given  case,  the  anamnesis  and 
accompanying  symptoms  should  be  taken  into  con- 
sideration in  addition  to  a  careful  examination  of  the 
patient.  In  one  case  the  manifestations  of  the  brain 
or  oblongata  are  decisive,  as  we  have  seen  in  Stokes- 
Adams  disease  and  the  Cheyne-Stokes'  phenomenon; 
in  another  case  it  is  that  form  of  dyspnoea  which  may 
be  followed  by  a  graphic  curve  of  respiration ;  in  others 
again  the  pulmonary  findings  by  auscultation  may 
assist,  as  for  instance,  the  signs  of  catarrh  decreasing 
from  the  base  of  the  lungs  to  the  apices,  as  observed  in 
the  dyspnoea  of  stasis.  In  many  cases  examination  of 
the  sputum  may  reveal  heart  failure  cells,  eosinophile 
cells,  erythrocytes  and  Curschmann's  spiral;  in  still 
others  the  examination  of  the  heart  itself  may  demon- 
strate enlargement  of  cardiac  dullness,  weakness  of  the 
heart  sounds,  or  the  reverse.  The  relation  to  blood 
pressure  has  already  been  considered.  The  various 
forms  of  arrhythmia  and  of  gallop  rhythm  which 
accompany  dyspnoea  should  be  subjected  to  a  special 


DYSPNCEA   AND    CYANOSIS  I27 

analysis.  In  one  case  the  pulse  during  a  paroxysm 
of  dyspnoea  is  irregular,  soft  and  compressible;  in 
another  retarded,  full  and  hard. 

ANEURISM   OF  THE  AORTA 

Dyspncea  and  cyanosis  in  aneurisms  of  the  aorta  are 
symptoms  of  compression  and  therefore  dependent 
upon  the  size  and  site  of  the  aneurism.  Compres- 
sion of  the  right  auricle  and  of  the  large  venous  trunks 
cause  the  most  intense  cyanosis,  which  may  attain 
an  exceedingly  high  degree  in  thrombosis,  endophle- 
bitis  and  especially  in  perforation  of  the  aneurism  into 
the  veins.  Cyanosis  together  with  dyspnoea  occurs 
when  the  pulmonary  artery  is  exposed  to  pressure  from 
aneurisms  and  there  is  consequent  hypertrophy  of  the 
right  ventricle.  The  compression  of  the  aorta  results 
in  a  similar  way,  and  in  large  aneurisms  also  the  un- 
common compression  of  the  pulmonary  veins.  The 
most  frequent  cause  of  dyspnoea  is  compression  of  the 
trachea  and  bronchi,  but  there  may  be  contributing 
factors  in  the  constriction  of  the  thoracic  space  from 
compression  of  the  auricles  and  the  pulmonary  vessels, 
also  from  the  work  thrown  upon  the  diaphragm  by 
large  aneurisms.  Finally  various  complications,  such 
as  inflammation  of  the  pleura,  pericardium  and  medi- 
astinum play  a  part  in  the  etiology  of  dyspnoea. 
Pains,  too,  occasioned  by  compression  of  the  intercos- 
tal nerves  of  the  brachial  plexus,  may  act  in  a  sim- 
ilar way.  Dyspnoea  and  cyanosis  in  the  final  phase 
of  aneurisms,  as  in  other  cardiac  affections,  are  per- 


128      DISORDERS   OF  RESPIRATION  AND  CIRCULATION 

fectly  explained  by  the  inefficiency  of  the  cardiac  func- 
tion. Compression  of  the  pneumogastric,  phrenic,  and 
recurrent  laryngeal  nerves  may  produce  symptoms 
which  recall  asthma  nervosum,  the  asthmatic  parox- 
ysms of  emphysema  and  hysterical  asthma.  In  these 
cases  it  should  be  remembered  that  the  asthmatic  par- 
oxysms in  aortic  aneurisms  belong,  as  a  rule,  to  the 
type  of  cardiac  asthma  and  that  dyspnoea  occurs  in  both 
phases  of  respiration ;  the  sputum  is  rich  in  cells,  often 
even  pigment  cells.  The  dyspnoea  outlasts  the  attack 
and  recurs  after  bodily  exertion. 

Dyspnoea  in  aneurisms  may  also  be  intermittent. 
Grossman  is  of  opinion  that  d3'-spnoea,  accompanied  by 
paralysis  of  the  vocal  cords  and  disappearing  in  a  rel- 
atively short  time,  is  characteristic  of  aneurisms  which 
develop  in  the  neighborhood  of  the  recurrent  laryn- 
geal. This  condition  is  in  contrast  to  the  malignant 
endothoracic  tumors  where  these  disturbances  are  ir- 
reparable. 

Dyspnoea  with  the  most  intense  cyanosis  of  the  face 
and  neck  with  positive  venous  pulse  and  hum  over  the 
aorta,  with  edema  of  the  upper  half  of  the  body,  while 
the  lower  half  is  unaffected,  occurs  in  perforations  of 
aneurisms  of  the  aorta  into  the  superior  vena  cava.  In 
perforating  aneurisms  of  the  aorta,  cyanosis  may  be 
relatively  absent  in  spite  of  the  most  marked  dyspnoea 
and  of  violent  pains  in  the  cardiac  region,  if  the  bleed- 
ing takes  place  slowly  and  progressive  anemia  devel- 
ops. This  has  been  obser\'ed  in  dissecting  aneurisms 
where  the  blood  is  retained  by  the  vascular  membranes. 


DYSPNOEA   AND    CYANOSIS  \I2g 

Even  in  perforations  into  the  pulmonary  artery  cyan- 
osis may  be  absent.  This  was  shown  by  Mager,  in 
whose  case,  after  the  estabhshment  of  a  communication 
between  the  aorta  and  the  pulmonary  artery,  only  a 
small  quantity  of  aortic  blood  flowed  into  the  pulmon- 
ary artery. 

ANEURISM    AND    SCLEROSIS    OF    THE    PULMONARY 
ARTERY 

Aneurisms  of  the  pulmonary  artery  are  exceedingly 
rare.  They  are  caused  by  the  atheromatous  process 
within  the  artery,  and  also  in  severe  mitral  stenosis  in 
consequence  of  the  increased  pressure  in  the  pulmon- 
ary arterial  system.  If  there  is  pulsation  in  the  second 
left  intercostal  space,  with  corresponding  dullness  and 
absence  of  the  second  sound  pointing  to  an  affection 
of  the  pulmonary  valve,  and  especially  the  presence  of 
diastolic  murmurs,  the  possibility  of  an  aneurism  of 
the  pulmonary  artery  should  be  considered.  In  a  case 
of  aneurism  of  the  pulmonary  artery  observed  by 
Skoda,  which  during  life  presented  itself  under  the 
mask  of  a  mitral  insufficiency,  there  was  increased  car- 
diac dullness,  systolic  murmur  over  the  left  ventricle 
which  was  transmitted  towards  the  right  ventricle  and 
the  base  of  the  heart,  weak  cardiac  impulse,  diminished 
diuresis  and  dropsy.  The  pulmonary  sounds  were 
scarcely  audible  and  there  was  dyspnoea  and  marked 
cyanosis. 

In  sclerosis  of  the  pulmonary  artery  even  without 


130      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

aneurismal  dilatation  there  was,  according  to  the  case 
pubHshed  by  Klob  and  Romberg,  during  life  consider- 
able cyanosis  with  hypertrophy  of  the  right  ventricle, 
systolic  murmur  at  the  apex,  accentuated  second  pul- 
monic sound,  and  small,  soft,  radial  pulse.  The  re- 
markable feature  of  these  cases  is  the  extraordinarily 
deep  cyanosis  with  a  complete  absence  of  edema  until 
death. 


IV 

DYSPNCEA  AND  CYANOSIS  IN  NEUROSES 
OF  THE  HEART 

CARDIAC  ASTHMA 

Dyspnoea  during-  bodily  overexertion,  especially 
muscular,  is  materially  different  from  those  attacks 
of  paroxysmal  dyspnoea  which  occur  suddenly  and 
without  previous  warning  in  individuals  who  never 
were  dyspnoeic  before  and  which  subside  just  as  sud- 
denly. Strictly  speaking,  these  sudden  paroxysms  of 
dyspnoea  should  not  be  looked  upon  as  an  exagg^era- 
tion  of  difficulties  of  breathing  already  existing  in  car- 
diac lesions,  as  they  form  a  symptom-complex  of  their 
own,  similar  to  bronchial  asthma.  Hofmann  is  cor- 
rect in  placing  cardiac  asthma  in  a  line  parallel  with 
stenocardia.  Cardiac  asthma,  like  stenocardia,  can  be 
regarded  as  a  neurosis  of  the  cardiac  nerve.  To  ex- 
plain this  polymorphism  of  stenocardic  parox^ysms 
and  their  radiating  phenomena  we  have  assumed  the 
existence  of  a  circle  which  connects  the  sympathetic 
ganglia  by  their  communicating  branches  with  the  spi- 
nal cord  and  in  which  both  primary  and  reflex  pro- 
cesses may  take  place.  For  a  stenocardic  attack  to 
be  produced,  it  makes  no  difference  according  to  our 
theory  whether  the  causative  irritation  originates  in 
the  end  apparatus,  i.  e.,  in  the  sensitive  organs  of  the 

131 


132      DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

coronary  arteries,  in  the  transit  stations,  i.  e.,  the  car- 
diac nerves,  in  the  communicating  branch,  or  in 
the  central  apparatus  in  the  spinal  cord.  Cardiac 
asthma  must  be  regarded  in  the  same  way  as  a  neurosis 
of  the  pulmonary  or  cardiac  plexus,  but  the  tracts, 
whose  irritation  produces  dyspnoea,  are  different  from 
those  active  in  stenocardia.  The  irritation  of  the  cen- 
trifugal tract  may  be  answered  by  vascular  constriction 
or  dilatation  in  the  lungs  and  bronchi,  so  that  the 
oppression  and  agony  find  an  explanation  in  an 
implication  of  the  centripetal  tracts  of  the  pneumo- 
gastric  causing  an  excitation  of  the  spinal  cord  and 
the  medulla  oblongata.  Perhaps  there  are  quite  dis- 
tinct groups  of  cardiac  ganglia  which  form  the  end 
apparatus  of  this  circle,  the  excitation  of  which  is  able 
by  purely  anatomical  processes  to  disturb  the  equilib- 
rium of  the  heart;  in  other  cases  also,  there  are 
reflex  irritations  of  the  central  nervous  system  which 
contribute  to  the  production  of  the  asthmatic  shock. 

PAROXYSMAL  TACHYCARDIA 

The  characteristic  stigmata  of  cardiac  asthma,  its 
sudden  appearance  and  equally  sudden  disappearance, 
are  characteristic  of  another  neurosis,  namely,  parox- 
ysmal tachycardia.  In  the  pure,  uncomplicated  cases 
of  paroxysmal  tachycardia,  respiration  is,  as  a  rule, 
undisturbed.  The  complexion  is  more  pale  than  cy- 
anotic, and  the  respiratory  quiet  together  with  the  neg- 
ative pulmonary  findings  form  a  striking  contrast  to 
the  stormy  action  of  the  heart.     In  protracted  parox- 


DYSPNCEA   AND   CYANOSIS  133 

ysms,  however,  cardiac  inefficiency,  congestion  of  the 
lungs,  dyspnoea,  cyanosis,  congestion  of  the  liver,  as- 
cites, and  anasarca  may  develop  as  a  sequel  to  dilata- 
tion of  the  heart.  If,  however,  paroxysmal  tachy- 
cardia occurs  in  individuals  whose  hearts  were  not 
normal  prior  to  the  attack,  as,  for  instance,  in  mitral 
stenosis,  myocarditis  or  pericardial  adhesions,  then  the 
manifestations  of  cardiac  inefficiency  with  dyspnoea 
and  deep  cyanosis  may  occur  at  an  early  stage. 


V 

DYSPNCEA   AND   CYANOSIS   IN   DISEASES 
OF  THE  GASTRO-INTESTINAL  TRACT 

DISEASES   OF  THE  STOMACH 

Special  attention  should  also  be  given  to  the  mani- 
festations on  the  part  of  the  stomach  and  intestine. 
In  some  cases  of  masked  forms  of  angina  pectoris 
with  radiation  into  the  esophagus,  esophagismus  and 
dysphagia,  vomiting,  pains  in  the  epigastrium,  diffi- 
culty of  breathing  and  oppression,  occupy  the  chief 
place.  In  another  case  it  is  the  epigastralgia  due  to  the 
congestion  of  liver  and  stomach,  which  accompanies 
the  dyspnoea.  This  is  the  result  of  the  inefficiency 
of  the  right  ventricle  in  cyanotic  patients  and  gives 
a  strange  aspect  to  the  general  picture. 

DISEASES    OF   THE    LIVER  AND    GALL   BLADDER 

Dyspnoea  from  the  toxic  products  of  metabolism, 
which  should  be  rendered  harmless  by  the  liver  and 
kidney,  offers  great  difficulty.  The  clinical  picture  of 
toxic  dyspnoea  due  to  inefficiency  of  the  renal  function, 
recalls  uremia.  Not  less  important  for  rendering  harm- 
less the  toxins  is  the  liver.  Dogs  with  Eck's  fistula 
according  to  several  observations  become  dyspnoeic 
and  refuse  to  eat  meat,  which  permits  the  inference 
that  alimentary  intestinal  toxins  are  capable,  after  ex- 

134 


DYSPNCEA   AND    CYANOSIS  I35 

elusion  of  the  action  of  the  liver,  of  exciting  the  center 
of  respiration.  In  the  pathology  of  dyspnoea  in  the 
human  subject  the  liver  also  seems  to  play  a  part, 
especially  when  there  is  renal  inefficiency.  The  cases 
in  which  insufficiency  of  hepatic  function  through  de- 
ficient action  on  the  intestinal  toxins  might  be  held 
responsible  for  the  origin  of  dyspnoea  are  hinted  at 
in  the  literature,  but  insufficiently  observed  and  de- 
scribed. And  yet  it  would  be  important  to  go  more 
thoroughly  into  a  question  which  is  full  of  value  both 
for  theory  and  practice.  In  all  cases  of  dyspnoea,  the 
character  of  which  points  to  a  toxic  causation,  a  thor- 
ough examination  of  the  hepatic  and  renal  functions 
should  be  made  by  modem  methods  of  investigation. 
From  a  clinical  point  of  view,  those  cases  are  of 
special  importance  in  which  cardio-pulmonary  dis- 
turbances are  present  in  affections  of  the  stomach, 
intestines  and  gallducts,  as  dilatation  of  the  right 
heart,  gallop  rhythm  with  maximum  intensity  behind 
the  sternum  and  in  many  cases  accentuation  of  the 
second  pulmonic  sound.  Such  cases  have  been  ob- 
served and  described  by  Potain.  It  is  a  question 
whether  in  these  cases  we  have  to  deal  with  a  reflex 
spasm  of  the  pulmonary  vessels  with  increase  of  pres- 
sure and  secondary  inefficiency  of  the  right  ventricle, 
as  occurs  in  gallstone  colics,  or  with  a  toxic  influence 
upon  the  vasomotors  of  the  lungs,  exercising  a  similar 
effect  upon  the  right  heart.  In  any  case,  the  forms  of 
dyspnoea  In  which  there  Is  simultaneous  disturbance 
of  digestion,  such  as  vomiting,  diarrhea,  dilatation  of 


136      DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

the  stomach,  pyrosis,  claim  especial  interest.  It  is 
possible  that  the  poisons  developed  in  the  diseased 
gastro-intestinal  tract  exert  a  specific  action  upon  the 
vasomotors  of  the  lungs  and  lead  to  a  secondary  eleva- 
tion of  the  blood  pressure  in  the  pulmonary  vessels, 
an  assumption  somewhat  strengthened  by  a  few  ex- 
periments on  animals.  An  excellent  example  of  the 
relations  between  the  liver  and  lungs  and  the  heart  are 
those  asthmatic  paroxysms,  frequently  associated  with 
agonizing  cardiac  arrhythmia  of  the  type  of  extra-sys- 
tole, which  occur  with  an  attack  of  gallstones  and 
usually  disappear  immediately  after  a  gallstone  colic 
and  the  passage  of  the  stone,  without  leaving  any  evi- 
dence of  trouble  behind.  From  these  examples  it  is 
evident  that  in  practice  there  are  several  forms  of 
cardiac  dyspncea  and  that  frequently  in  one  and  the 
same  individual  several  components  may  be  active, 
which  accounts  for  the  enormous  difficulties  en- 
countered in  both  the  clinical  analysis  and  in  the 
therapy  to  be  selected. 


VI 

DYSPNCEA  AND  CYANOSIS  IN  INFECTIOUS 
DISEASES 

The  cause  of  dyspnoea  and  cyanosis  occurring  in  the 
course  of  infectious  diseases  lies  in  their  intimate  con- 
nection with  the  pathogenesis  of  these  affections.  The 
causes  of  infection  may  lead  to  pathological  changes 
in  the  lungs  and  heart  through  local,  regional  and 
metastatic  channels  as  is  the  case  with  most  bacteria, 
or  to  their  multiplication  in  the  blood,  as  in  anthrax. 
They  may  act  as  deoxygenizers  and  thereby  interfere 
with  the  interchange  of  gases,  or  they  may  manifest 
their  action  by  toxins,  which  possess  a  chemical  affin- 
ity for  organic  cells  susceptible  to  poison,  and  to  which 
they  attach  themselves.  The  toxins  of  tetanus  and 
botulism  select  certain  neurons  of  the  nervous  system, 
the  diphtheria  toxin  acts  on  the  nerve  fibers  of  cer- 
tain areas,  also  upon  the  heart  and  the  vessels.  Both 
toxins  and  endotoxins  (which  result  from  the  decay 
of  the  bacterial  bodies)  may  produce  distant  effects 
through  the  circulation  as  a  polyneuritis  or  grave  ob- 
struction to  respiration  and  circulation  by  the  toxic 
degeneration  of  various  organs  (kidney,  liver,  heart, 
etc.).  Influenza  and  cholera  furnish  proofs  of  both. 
Secondary  infections  of  the  organs  injured  by  toxins 
contribute  their  share  in  intensifying  and  complicating 

137 


138      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

the  local  change  of  tissue  and  their  distant  effect.  The 
hemolytic  effect,  too,  of  some  bacteria  Is  also  to  be 
taken  into  account  as  a  cause  of  toxic  injury,  as  is 
well  known  in  the  case  of  staphylococci  and  strepto- 
cocci. 

DIPHTHERIA 

The  chief  factor  in  the  causation  of  dyspnoea  in 
diphtheria  is  the  localization  of  the  process  in  the 
larynx  or  trachea  and  in  descending  diphtheria,  the 
involvement  of  the  bronchi.  If  the  pulmonary  paren- 
chyma is  involved  in  the  way  of  multiple  bronchopneu- 
monic  foci,  the  manifestations  will  relatively  increase. 
Aside  from  the  localization  in  the  respiratory  appara- 
tus, other  factors  are  to  be  considered  in  the  develop- 
ment of  threatening  symptoms,  namely  cardiac  weak- 
ness caused  by  degeneration  of  the  muscular  substance, 
hemorrhage  in  the  myocardium,  changes  in  the  pneu- 
mogastric  nerve  including  its  motor  nucleus,  and  also 
vaso-paralysis  with  progressively  lessening  blood  pres- 
sure. These  changes  are  attributed  in  the  acute  stages 
to  the  deleterious  effect  of  the  diphtheria  toxin,  while 
the  late  paralyses,  In  which  degeneration  of  the  per- 
ipheral nerves  manifests  itself,  are  assumed  to  be  due 
to  the  action  of  toxins.  In  diphtheria  which  runs  its 
course,  as  a  general  Intoxication  there  may  be  tachy- 
pnoea  up  to  sixty  a  minute,  which  is  usually  a  premor- 
tal sign. 

MEASLES^  SCARLET  FEVER  AND  VARIOLA 

The  occurrence  of  dyspnoea  in  measles  has  already 
been  described.     In  scarlet  fever,  affections  of  the  air- 


DYSPNCEA   AND   CYANOSIS  I39 

tract  and  lungs  are  less  frequent  than  in  measles. 
Dyspnoea  and  cyanosis  are  observed  in  malignant 
forms  of  scarlet  fever  and  occur  as  the  result  of  several 
factors,  as  complications  with  pleuritis,  endocarditis, 
pericarditis  and  myocarditis,  and  especially  in  the  acute 
stage  of  hemorrhagic  scarlet  fever  and  in  complications 
with  diphtheria ;  in  the  later  stage  with  dropsy,  hydro- 
thorax  and  edema  of  the  glottis  consequent  upon  sec- 
ondary nephritis.  Swelling  of  the  face  develops  from 
involvement  of  the  cervical  lymphatic  glands  and  the 
cervical  cellular  tissue,  and  cyanosis  occurs  with  con- 
siderable increase  of  respiration,  affecting  speech  and 
deglutition.  In  a  similar  way  dyspnoea  and  cyanosis 
in  variola  may  be  occasioned  by  localization  of  the  af- 
fection in  the  respiratory  apparatus ;  by  an  affection  of 
the  larynx,  edema  of  the  glottis,  or  by  extension  of 
the  variola  to  the  large  bronchi ;  also  by  hemorrhagic 
exudates  in  the  lungs,  pleural  cavities,  pericardium  or 
mediastinum,  and  finally  by  injury  to  the  circulatory 
apparatus.  The  skin  assumes  a  bluish  black  coloration 
from  the  cyanosis  and  from  the  hemorrhages  In  the 
derma  (smallpox).  Dyspnoea  may  exist  in  these  cases 
and  without  any  change  in  the  respiratory  or  circula- 
tory systems. 

MALARIA 

In  malaria,  during  the  stage  of  chill,  there  may  be 
considerable  dyspnoea  with  coughing,  oppression,  pre- 
cordial fear,  even  though  the  circulation  is  not  materi- 
ally Impaired,  but  It  disappears  together  with  the 
fever.     These  respiratory  disorders,  which  are  accom- 


140      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

panied  by  profound  cyanosis,  are  usually  caused  by 
hyperemia  of  the  lungs  and  bronchi.  Intermittent 
dyspnoea  occurs  in  the  pernicious  forms  of  malaria 
which  are  described  as  malarial  pneumonia  and  malar- 
ial pleuritis.  Rare  complications  are  endocarditis  and 
rupture  of  the  heart. 

TYPHOID,    TYPHUS,    RELAPSING    FEVER 

Dyspnoea  may  be  occasioned  by  manifold  causes  in 
typhoid.  The  increased  frequency  of  respiration  may 
be  of  febrile  origin.  Difficulties  of  respiration  may 
be  the  result  of  obstruction  of  the  nostrils,  while  grave 
dyspnoea  is  caused  by  ulcerative  and  perichondritic  pro- 
cesses of  the  larynx,  laryngeal  edema  and  croup  of 
the  respirator}'  tract.  In  extensive  multiple  atelect- 
tasis,  in  hypostasis  and  pneumonic  affections,  in  edema 
of  the  lungs,  in  hemorrhages  of  the  lungs  and  pleu- 
ritis, dyspnoea  with  increased  frequency  of  respiration 
and  cyanosis  are  easily  explainable.  An  intense  dys- 
pnoea occurs  in  central  swelling  of  the  bronchial 
glands  with  hemorrhages  into  the  substance  and  into 
the  surrounding  cellular  tissue,  and  it  is  often,  espe- 
cially in  children,  out  of  proportion  to  the  catarrhal 
manifestations  of  the  lungs  (pneumot}'phoid).  Myo- 
carditis, endocarditis,  and,  in  rare  cases,  pericarditis, 
may  cause  these  same  symptoms.  A  high  degree  of 
meteorism  may  influence  respiration  and  circulation 
by  pushing  up  the  diaphragm,  and  embolism  of  the 
pulmonary  arter}^  may  lead  to  the  well-known  and 
already  detailed  picture. 

There  is  frequently  dyspnoea  and  cyanosis  In  typhus 


DYSPNCEA   AND   CYANOSIS  I4I 

fever  owing  to  cardiac  weakness  and  to  the  changes 
in  the  respiratory  tract, — ^bronchitis,  pneumonia,  and 
sometimes  edema  of  the  glottis. 

In  relapsing  fever,  severe  dyspnoea  may  be  present 
with  exceedingly  high  frequency  of  the  pulse,  fear  and 
prostration  during  the  acme  of  the  disease,  and  shortly 
before  the  remission  with  negative  findings  in  the  res- 
piratory organs,  and  it  may  disappear  rapidly  with  the 
remission.  When  complicated  with  endocarditis  and 
pneumonia,  dyspnoea  and  cyanosis  may  occur  in  the 
same  manner  as  in  typhoid. 

ERYSIPELAS^  INFLUENZA 

In  erysipelas  of  the  skin  as  well  as  in  internal  ery- 
sipelas, dyspnoea  and  cyanosis  occur  from  localization 
of  the  affection  in  the  respiratory  area.  Exacerbation 
of  the  existing  toxo-infectious  manifestations  and  the 
appearance  of  dyspnoea  generally  indicate  pneumonia, 
which  usually  takes  a  rapid  course  and  causes  death 
with  signs  of  asphyxia  and  coma. 

There  are  conditions  of  suffocation  with  cyanosis,  in 
influenza,  sometimes  without  any  corresponding,  ob- 
jectively demonstrable  changes  in  the  lung.  They  are 
attributed  to  functional  disturbances  in  the  area  of  the 
pneumogastric,  or  to  congestion  of  the  lungs.  Dys- 
pnoea and  cyanosis  may  appear  at  an  early  stage  of 
bronchopneumonia,  which  results  from  the  confluence 
of  multiple  bronchopneumonic  foci,  with  grave  gen- 
eral symptoms,  prostration  and  great  frequency  of 
pulse,  and  they  sometimes  bear  no  proportion  to  the 


142      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

extent  of  the  pulmomry  infiltration.  The  same  was 
obsen'-ed  in  Finkler's  contagious  streptococcus  pneu- 
monia which  appeared  as  a  house-epidemic  and  was 
similar  to  influenza.  Marked  dyspnoea  with  tachy- 
pnoea  and  small,  weak  pulse  stood  in  the  foreground  of 
the  clinical  picture. 

PLAGUE 

In  the  plague,  dyspnoea  and  cyanosis  occur  from 
various  causes.  Rapidly  developing  cervical  buboes 
may  cause  asphyxiation,  and  the  swelling  of  the  lym- 
phatic glands  in  the  thoracic  cavity  may  produce  dys- 
pnoea with  oppression  and  an  annoying  dry  cough. 
Both  primary  and  secondary  plague-pneumonia,  re- 
sulting from  ulcerated  tonsillary  buboes,  are  accom- 
panied by  bloody  expectoration  containing  many  plague 
bacilli;  here  dyspnoea  and  cyanosis  occur  at  an  early 
stage  and  are  extreme. 

ANTHRAX 

Cyanosis  with  intense  dyspnoea,  fever,  viscid  and 
frequently  bloody  expectoration,  which  may  have  the 
appearance  of  prune  juice,  with  contractile  pains  in 
the  chest,  intensified  by  movement,  with  a  sensation  of 
fear  and  cold  in  the  internal  organs,  not  infrequently 
with  full  consciousness  until  death,  occur  in  those 
forms  of  anthrax  in  which  the  lungs  and  pleura  are 
especially  infected  with  numerous  foci  of  bacilli.  The 
cause  of  the  cyanosis  in  these  cases  is  not  connected 
with  cardiac  inefiiciency,  since  the  heart,  in  contrast 
to  other  infectious  diseases,  does  not  as  a  rule  undergo 


DYSPNOEA   AND   CYANOSIS  143 

fatty  degeneration  in  anthrax,  but  is  usually  found  to 
be  healthy.  Simultaneous  intestinal  manifestations 
(anthrax  intestinalis)  and  the  demonstration  of  the 
bacilli  in  the  blood  aid  in  the  diagnosis.  The  poly- 
morphism of  the  pathological  picture,  which  depends 
chiefly  on  the  accumulation  of  bacilli  in  the  various 
organs,  makes  it  improbable  that  the  anthrax  bacilli 
produce  a  specific  toxin  which  attacks  vital  organs,  as 
is  the  case,  for  instance,  in  diphtheria.  Hoffa  and 
Martin  have,  however,  obtained  a  poisonous  substance 
from  pure  cultures  which  in  animals  produced  grave 
general  manifestations  and  also  enlargement  of  the 
spleen.  The  cause  of  cyanosis  in  anthrax  is  supposed 
to  be  due  to  the  accumulation  of  bacilli  in  the  capil- 
lary blood  (capillary  thrombosis),  and  the  subtraction 
of  oxygen  from  the  blood  by  the  bacilli. 

MALIGNANT  EDEMA 

Similarly  to  primary  and  secondary  pulmonary  an- 
thrax, which  emanates  from  a  local  skin  affection,  cya- 
nosis with  difficulty  in  breathing  and  loss  of  strength 
occurs  in  the  "  Hadernkrankheit,"  which  is  caused  by 
the  inhalation  from  "  Hadern,"  or  old  rags,  and  is 
found  in  persons  working  in  paper  factories.  This  in- 
fectious disease  is  accompanied  by  headache,  sensation 
of  oppression,  spastic  cough  with  viscid  expectoration, 
under  the  picture  of  a  lobar  pneumonia.  Thoracic 
pain,  however,  is  frequently  absent,  the  temperature 
remains  low,  the  sensorium  is  unimpaired,  while  the 
physical   manifestations   in   the   lungs   are   relatively 


144        DISORDERS    OF   RESPIRATION    AND    CIRCULATION 

slight.  Although  the  "  Hadernkrankheit "  is  caused 
in  many  cases  by  the  inhalation  of  "  Hadern  "  dust, 
containing  anthrax  spores,  in  other  cases,  described  by 
Kranhals,  it  is  not  the  anthrax  bacillus,  but  the  bacil- 
lus of  malignant  edema  which  causes  this  infectious 
disease.  The  edema  bacillus,  having  once  entered 
the  lungs,  spreads  into  the  connective  tissue  of  the  pleu- 
ral, mediastinal,  pericardial  and  bronchial  glands  in 
the  same  way  as  it  does  into  subcutaneous  connective 
tissue.  In  other  cases  there  is  probably  a  mixed  in- 
faction  of  anthrax  and  malignant  edema,  perhaps 
also  of  other  fontis  of  septicemia,  which  would  suffi- 
ciently explain  the  multiformity  of  the  clinical  symp- 
toms. 

GLANDERS 

In  glanders,  dyspnoea  and  cyanosis  depend  upon  the 
localization  of  the  process  in  the  respiratory  and  cir- 
culatory tracts.  If  the  affection  is  localized  in  the 
respiratory  tract,  especially  in  the  lungs,  difficulty  in 
breathing  is  frequent.  This  may  be  intensified  in  the 
further  course  of  the  disease  to  pronounced  dyspnoea 
with  considerable  cough  and  abundant  expectoration, 
often  thin  and  serous,  later  more  purulent,  sometimes 
bloody  and  putrid,  in  consistency  similar  to  nasal  se- 
cretion. Localization  of  abscesses  In  the  respiratory 
muscles  and  In  the  heart  are  likewise  of  great  im- 
portance. 

TRICHINOSIS 

Cyanosis  and  dyspnoea  also  occur  In  trichinosis,  if 
the  parts  invaded  are  the  diaphragm  and  the  thoracic 


DYSPNCEA   AND   CYANOSIS  145 

muscles.  When  the  trichinae  were  chiefly  located  in 
the  muscular  substance  of  the  diaphragm,  Traube  ob- 
served cyanosis  with  a  costal  type  of  respiration,  op- 
pression of  the  chest  and  a  very  frequent  pulse.  If 
the  trichinosis  is  situated  in  the  respiratory  muscles, 
dyspnoea,  with  difficult  inspiration  and  extraordinary 
acceleration  of  respiration,  may  assume  the  character 
of  asthmatic  paroxysms,  which  not  infrequently  are 
the  cause  of  death.  High  fever,  profuse  perspira- 
tion with  miliary  eruptions,  rigidity  of  the  muscles  of 
the  entire  body,  which  are  sensitive  to  pressure,  con- 
tractions of  almost  all  articulations,  turgescence  of  the 
face  and  edema  of  the  eyelids,  also  the  eosinophllia 
of  the  blood  characteristic  of  trichinosis,  may  be  men- 
tioned as  noteworthy  signs  of  the  disease.  Cyanosis 
and  dyspnoea  caused  by  affections  of  the  respiratory 
muscles,  may  be  intensified  by  disseminated  broncho- 
pneumonia which  frequently  accompanies  trichinosis, 
and  is  often  occasioned  by  occlusion  of  the  smallest 
branches  of  the  pulmonary  artery. 

ASIATIC   CHOLERA^    PERITONITIS 

In  Asiatic  cholera,  true  dyspnoea  is  a  very  rare  oc- 
currence, not  taking  into  account  the  feeling  of  oppres- 
sion and  fear,  palpitation  and  pressure  in  the  cardiac 
region.  Secondary  affections  of  the  respiratory  or- 
gans, like  bronchitis  and  pneumonia,  are  not  frequent 
even  in  the  typhoid  state  of  cholera.  On  the  other 
hand,  cyanosis  of  the  lips,  ears  and  extremities,  with 
small  or  no  pulse,  is  the  dominating  symptom  in  the 


146      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

asphyctic  stage  of  cholera.  The  lungs  become  anemic 
in  consequence  of  the  weakness  of  the  right  heart,  the 
arteries  are  empty.  The  veins  are  filled  with  black 
blood,  which,  in  consequence  of  the  decrease  of  the  vis 
a  fergo  from  weakness  of  the  left  ventricle,  is  tarlike, 
thick  from  loss  of  water,  incapable  of  circulation,  and 
does  not  become  red  when  exposed  to  the  air.  In  spite 
of  the  increasing  viscosity  and  venosity  of  the  blood 
and  notwithstanding  the  impairment  of  the  pulmonary 
circulation,  there  is  no  reaction  to  respiratory  irritation. 
The  recurrence  of  cyanosis  with  coldness  of  the  ex- 
tremities in  the  reactionary  stage  of  cholera  (cholera 
t}^hoid)  is  a  sign  of  an  exacerbation  which  not  infre- 
quently leads  to  death  after  a  short  period  of  apparent 
amelioration. 

While  dyspnoea  practically  never  occurs  in  cholera, 
difficulty  in  breathing  may  develop  in  the  course  of 
cholera-typhoid  from  local  inflammatory  affections  of 
the  respiratory  organs  (laryngeal  and  bronchial  af- 
fections, pneumonic  infarcts,  edema  of  the  lungs). 
In  isolated  cases  of  cholera-nephritis,  there  may 
even  be  violent  dyspnoea  which  reminds  one  of  uremia. 
In  cholera  the  moist  skin  is  never  absent,  but  when 
this  is  pronounced  and  there  is  cyanosis,  it  is  a  sign 
of  the  worst  possible  import,  as  is  the  presence  of  dys- 
pnoea, which,  however,  occurs  only  in  rare  cases.  The 
same  is  true  of  cholera  nostras,  except  that  in  the  ma- 
jority of  cases  cyanosis  is  not  so  marked,  the  skin  is 
somewhat  paler  and  the  mucous  membranes  livid.  In 
severe  cases  of  dysentery,  lowered  temperature  and 


DYSPNOEA   AND   CYANOSIS  I47 

dryness  and  cyanosis  of  the  skin  and  mucous  mem- 
branes are  prognostically  unfavorable  signs.  Many 
cases  of  dysentery  complicated  with  peritonitis  and 
gastro-enteritis  present  the  complex  picture  of  cholera 
asphyctica, — diarrhea  and  vomiting, — associated  with 
coldness  of  the  extremities  and  pulselessness. 

The  final  phase  of  general  peritonitis  is  likewise 
characterized  by  superficial  and  accelerated  respira- 
tion, singultus,  vomiting,  change  in  the  facial  contour 
with  cyanosis  of  the  nose,  ears  and  extremities. 


VII 

DYSPNCEA  AND  CYANOSIS  DUE  TO 
POISONS 

In  cases  of  poisoning  several  factors  come  into  con- 
sideration to  explain  the  dyspnoea  and  cyanosis  as 
injury  to  the  respiratory  and  circulatory  tracts,  and 
blood  changes  which  render  the  blood  less  fit  or  com- 
pletely unfit  for  the  interchange  of  gases.  The  res- 
piratory apparatus  may  be  affected  also  in  various 
ways:  the  center  for  respiration  may  be  excited  or 
paralyzed,  the  peripheral  respiratory  muscles  and  the 
peripheral  nerves,  especially  their  intramuscular  ter- 
minations involved,  or  there  may  be  secondary  changes 
in  the  respiratory  tract. 

MORPHIN,   CHLOROFORM,   ALCOHOL,   TOBACCO 

The  chief  poison  affecting  the  center  for  respiration 
is  morphin,  which  reduces  its  excitability  and  finally 
paralyzes  it,  so  that  even  an  intense  venosity  of  the 
blood  is  no  longer  capable  of  producing  respiratory 
movements.  In  poisoning  with  morphin,  therefore, 
the  respiration  becomes  slow  and  irregular,  accom- 
panied by  rales,  and  the  skin  is  livid  or  a  dark  cyanotic 
hue. 

Chloroform  has  a  similar  effect;  first  it  paralyzes 

148 


DYSPNCEA  AND   CYANOSIS  149 

the  cerebral  cortex  and  then  the  center  for  respiration. 
In  the  third  stage  of  chloroform  poisoning  the  sur- 
geon quickly  recognizes  the  following  manifestations: 
syncope,  asphyxia,  stoppage  of  respiration  with  cy- 
anosis and  dilated  pupils,  cessation  of  pulse  and  of 
hemorrhage  during  operation.  In  alcoholic  intoxica- 
tions there  is  sopor,  general  anesthesia,  deep  stertorous 
respiration,  small,  frequent,  soft  pulse,  cyanosis  of  the 
skin  and  mucous  membranes,  coolness  of  the  extrem- 
ities. In  the  gravest  cases  there  is  dilatation  of  the 
pupils  without  pupillary  reaction,  in  the  less  severe 
cases  they  are  contracted.  Similar  conditions  may 
prevail  in  poisoning  with  ether  and  laughing  gas. 

In  acute  tobacco  poisoning,  there  is  vomiting,  ver- 
tigo, sweating,  spasms,  palpitation,  rapid  and  irreg- 
ular pulse,  deep  dyspnoea  with  stertorous  breathing, 
edema  of  the  lungs  and  cessation  of  breathing.  The 
picture  of  solanin  poisoning  is  similar. 

BELLADONA,  HYOSCYAMUS,  CALABAR  BEAN, 
PHYSOSTIGMIN,  ACONITE,  COLCHICUM 

In  the  multiform  picture  of  poisoning  with  bella- 
donna and  hyoscyamus,  dyspnoea  and  cyanosis  occur 
only  as  terminal  manifestations,  occasioned  by  paraly- 
sis of  the  center  of  respiration  and  of  the  heart.  Also 
intoxications  with  calabar  bean  and  physostigmin, 
which  are  accompanied  by  contraction  of  the  pupils, 
may  cause  dyspnoea  with  diminishing  frequency  and 
finally  paralysis  of  respiration,  in  addition  to  mani- 
festations on  the  part  of  the  intestinal  tract.     A  sim- 


150      DISORDERS   OF  RESPIRATION  AND   CIRCULATION 

ilar  picture  with  grai'e  d3'spnoea  and  asphyctic  spasms 
is  presented  by  aconite  poisoning,  for  which  dilatation 
of  the  pupils  is  characteristic.  Colchicum  intoxica- 
tions recall  the  picture  of  cholera  or  of  arsenical  poi- 
soning, and  here  cyanosis  with  small,  scarcely  percepti- 
ble pulse,  coldness  of  the  extremities  with  complete 
consciousness  occupy  the  foreground. 

STRYCHNIN,  CAMPHOR,  CURARE,  CONIUM 

The  principal  representative  of  the  poisons  which 
excite  the  respiratory  motor  ner\^es  is  strychnin.  In 
the  course  of  strychnin  intoxication  there  is  consider- 
able dyspnoea  with  cyanosis  and  edema  of  the  face 
with  prominent  eyeballs  in  consequence  of  the  tono- 
clonic spasm  of  the  respiratory  and  cervical  muscles 
and  the  inspirator}^  immobolization  of  the  thorax. 
Both  dyspnoea  and  anxiety  may  appear  before  the 
tetanic  paroxysms.  Dyspnoea,  due  to  spasm  of  the  re- 
spiratory muscles,  with  convulsions,  unconsciousness, 
vomiting,  profuse  perspiration,  small  and  frequent 
pulse  and  lowering  of  the  body  temperature  have  been 
obser\"ed  in  camphor  poisoning. 

In  poisons,  paralyzing  the  motor  terminals  of  the 
thoracic  and  diaphragmatic  nerves,  as,  for  instance, 
curare,  asph3rx:ia  is  easily  explainable  by  cessation  of 
respiration.  Cases  of  curare  poisoning  have  been  de- 
scribed in  which  death  ensued  within  a  few  minutes 
without  spasms,  because  the  poison  paralyzed  at  once 
the  nerve  terminals  of  the  musculature  of  both  trunk 


DYSPNCEA   AND    CYANOSIS  I5I 

and  extremities.  In  cases  where  the  trunk  muscles 
are  paralyzed  after  the  thoracic  muscles,  there  may  be 
general  convulsions  from  the  effect  of  the  asphyxiated 
blood.  Such  seems  to  be  the  case  in  conium  poison- 
ing, in  which  there  is  vertigo,  stupor,  weakness  of  the" 
heart  and  of  the  muscles  in  conjunction  with  twitch- 
ing of  the  extremities.  Respiration  becomes  labored 
and  retarded,  there  is  dyspnoea  and  finally  cessation 
of  respiration.  An  ascending  paralysis  of  the  spinal 
cord  might  have  existed  in  the  case  of  Socrates  when 
he  drained  the  poisoned  cup,  because  he  was  able  to 
speak  and  bid  farewell  to  his  friends  although  the  mus- 
cles of  motion  and  sensation  were  parayzed. 

TETRODEN    FISH,    FUNGUS,   AGARIC   GNAT 

This  same  group  of  poisons,  which  paralyzes  the 
muscles  of  respiration,  also  includes  the  poison  of  the 
Japanese  tetroden  fish,  which  is  used  for  suicidal 
and  homicidal  purposes  and  on  shipboard  has  been 
the  cause  of  wholesale  sickness  with  fatal  termination, 
Fugu  poison,  which  is  prepared  from  tetroden  ova, 
shows  properties  similar  to  curare,  but  the  picture  of 
the  poisoning  after  the  ingestion  of  these  poisonous 
fish  varies  according  to  the  variety  of  the  species,  some 
cases  resembling  chloral  and  opium  poisoning,  and 
others,  belladonna  poisoning  or  botulism,  in  which 
mydriasis,  ptosis,  considerable  paroxysmal  dyspnoea 
with  dryness  in  the  throat,  dysphagia  and  disturbance 
of  vision  are  present.     In  fungus  poisoning  there  is, 


152      DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

aside  from  the  gastro-enteric  symptoms  and  mental 
disturbances  as  in  atropin  poisoning,  dyspnoea  with 
paroxysmal  attacks  of  suffocation,  and  stertorous 
breathing  owing  to  edema  of  the  lungs;  in  agaric 
gnat  poisoning  there  is  also  retardation  of  the  pulse. 

BARIUM  SALTS^  CORROSIVE  SUBSTANCES 

Intestinal  manifestations  with  slow  pulse,  dyspnoea, 
anxiety  and  coldness  of  the  extremities,  convulsions 
from  suffocation  and  paralysis  of  the  heart  occur  in 
intoxication  with  barium  salts.  In  poisoning  with 
corrosive  substances  like  sulphuric  acid,  nitric  acid,  hy- 
drochloric acid,  caustic  soda  and  bichlorid  of  mer- 
cury, there  are  difficulties  in  breathing,  especially  in 
cases  where  the  poison  cauterizes  the  lar^-nx  and  tra- 
chea, so  that  the  air  has  difficulty  in  gaining  access  to 
the  lungs,  owing  to  the  considerable  swelling  of  the 
mucous  membranes. 

The  well-known  symptoms  of  internal  poisoning  by 
caustic  ammonia,  i.  e.,  salivation,  vomiting,  diarrhea 
and  considerably  accelerated  respiration  may  also  oc- 
cur, if  the  poison  has  been  introduced  by  the  rectum. 
This  happened  in  a  case  under  my  observ^ation,  where 
a  patient  had  used  an  ammonia  enema  in  mistake  for 
glycerin.  There  was  swelling  of  the  buccal  mucous 
membrane  and  a  secondary  ulcerous  stomatitis  w^ith 
Vincent's  organisms  (spirochetse  and  fusiform  ba- 
cillus), as  seen  in  mercurial  stomatitis. 


DYSPNCEA   AND    CYANOSIS  153 

IRRITATING    GASES    AND    VAPORS 

Inhalations  of  irritating  gases  and  vapors,  as  chlo- 
rin.  bromin,  iodin,  hydrochloric  acid,  hydrobromic 
acid,  nitric  acid,  nitrous  acid,  ammonia,  etc.,  cause  dis- 
turbance of  respiration  by  reflex  spasm  of  the  glottis 
and  constriction  of  the  bronchioles,  means  of  defense, 
also  by  secondary  changes  in  the  mucous  membranes 
of  the  larynx  and  the  bronchi,  which  may  lead  to 
edema  of  the  glottis,  severe  bronchitis  and  lobar 
pneumonia.  Aside  from  the  local  manifestations, 
these  gases  may  also  produce  distant  effects  upon 
respiration  and  circulation  by  causing  injury  to  the 
heart,  to  the  center  for  respiration  and  by  direct  con- 
tamination of  the  blood. 

After  the  inhalation  of  a  concentrated  mixture  of 
carbon  dioxid,  dyspnoea  and  unconsciousness  may 
occur,  symptoms  analogous  to  those  of  suffocation^ 

DIGITALIS^  HELLEBORE  AND  VERATRUM 

Digitalis  and  hellebore  should  be  mentioned  among 
the  poisons  which  cause  dyspnoea  by  direct  action  upon 
the  cardiac  function.  Vomiting,  violent  headache, 
dimness  of  vision,  chromatopsy,  tinnitus  aurium,  faint- 
ing, cold  perspiration,  marked  muscular  weakness,  with 
consciousness  relatively  intact,  considerable  retardation 
of  pulse,  make  up  the  clinical  picture  of  these  intoxica- 
tions. General  cyanosis  with  sopor,  coma,  and  con- 
vulsions occur  with  reduction  of  the  body  temperature, 


154      DISORDERS   OF   RESPIRATION    AXD    CIRCULATION 

increase  of  pulse  frequency  and  arrhythmia.  There 
is  a  similarity  between  the  symptom-complex  of  digi- 
talis and  veratrum  poisoning,  except  that  the  gastric 
manifestations  with  salivation,  also  the  diminution  of 
cardiac  function  and  paralysis  of  the  center  for  respira- 
tion appear  more  rapidly  in  veratrum  poisoning. 

PHOSPHORUS 

In  phosphorus  poisoning,  cyanosis  due  to  the  en- 
gorgement of  the  venous  system  is  hidden  by  the  syn- 
chronous icterus.  The  labored  breathing  is  explained 
by  the  weakening  of  the  cardiac  function.  In  rare 
cases  dyspnoea  and  cyanosis  are  obsen^ed  from  a 
rupture  at  some  point  in  the  aorta  where  there  is  fatty 
degeneration. 

CARBON  MONOXID 

Blood  poisons  may  produce  dyspnoea  and  cyanosis 
in  that  they  render  the  blood  unfit  for  respiration,  both 
for  the  interchange  of  gases  and  the  transmission  of 
oxygen.  This  may  take  place  in  two  ways.  Either 
the  poison  absorbed  assimilates  with  the  hemoglobin 
without  changing  the  red  blood  corpuscles,  or  it  ef- 
fects a  change  in  the  oxyhemoglobin  of  the  red  blood 
corpuscles  with  or  without  their  destruction.  Met- 
hemoglobin  is  formed  in  the  first  combination  and  is 
equally  unfit  for  respiration  or  transmission  of  oxygen. 
The  best  known  representative  of  the  first  group  is 
carbonmonoxid,  which  displaces  the  oxygen  from  the 
oxyhemoglobin,  assimilates  wdth  hemoglobin  and 
forms  a  firmer  combination,  carbonmonoxidhemoglo- 


DYSPNCEA    AND    CYANOSIS  155 

bin,  which  is  incapable  of  either  oxydation  or  respira- 
tion. The  most  prominent  symptoms  in  this  intoxica- 
tion, therefore,  are  dyspnoea  with  impending  asphyxia, 
abnormally  high  frequency  of  pulse  and  decreasing 
blood  pressure,  sleepiness  and  diminished  reflex  excita- 
bility with  a  tendency  to  inflammatory  affections  of  the 
lungs.  In  the  soporific  stage,  respiration  may  be  regu- 
lar and  scarcely  affected,  or  there  may  be  intermissions 
in  the  respiration  and  death  follows  with  or  without 
terminal  convulsions.  Occasionally  clonic  and  tonic 
spasms  of  the  extremities  may  occur  early  with  tris- 
mus and  facial  spasms. 

In  carbonmonoxid  poisoning,  the  color  of  the  mu- 
cous membranes  and  of  the  skin  is  sometimes  bright 
red,  at  times  pale,  grayish  or  livid;  frequently  there 
is  hyperemia  in  spots  on  various  parts  of  the  body. 
Cyanosis  and  edema  occur  as  terminal  symptoms  only 
toward  the  end,  due  to  the  disturbance  of  circulation. 
Aside  from  its  effect  upon  the  hemoglobin,  carbonmon- 
oxid seems  to  exert  direct  toxic  effects  upon  the  ves- 
sels and  the  nerve  elements,  as  is  proved  by  the  nu- 
merous cases  of  histologically  demonstrated  affections 
of  the  central  and  peripheral  nervous  system  and  of  the 
vessels  (disseminated  encephalitis,  especially  of  the  cer- 
ebral ganglia,  sometimes  immediately  following  the 
poisoning).  In  an  eighteen-year-old  girl  poisoned  by 
illuminating  gas  and  treated  at  our  clinic  there  was, 
aside  from  unconsciousness  and  labored  breathing, 
edema  of  the  face,  hyperemia  of  the  skin  in  lim- 
ited areas,  small,  compressible  arrhythmic  pulse,  pupils 


156      DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

at  first  markedly  contracted  and  without  reaction,  ele- 
vation of  temperature,  tetaniform  spasms  of  the  upper 
extremities  and  pectoral  muscles,  exaggeration  of  the 
patellar  reflexes,  bilateral  Babinski  reflex,  sugar  and 
lactic  acid  in  the  urine.  After  two  days  of  uncon- 
sciousness there  was  a  rather  rapid  subsidence  of  all 
symptoms  and  recovery. 

SUBSTANCES    FORMING   METHEMOGLOBIN 

The  second  group  of  poisons  is  characterized  by 
the  formation  of  methemoglobin.  There  are  sub- 
stances which  change  oxyhemoglobin  into  methemo- 
globin without  destruction  of  the  red  blood  corpuscles, 
as  amylnitrit,  antifebrin,  kairin  and  nitrobenzol. 
Others  form  methemoglobin  and  change  the  structure 
of  the  red  blood  corpuscles,  as  the  chlorats,  nitrits,  and 
anilin.  In  some  poisons  the  formation  of  methemo- 
globin commences  at  an  earlier  stage  than  do  the 
changes  in  the  red  blood  corpuscles,  and  the  degree  of 
chemical  change  in  hemoglobin  is  not  always  propor- 
tionate to  the  morphological  injury  to  the  cell  body  of 
the  red  blood  corpuscles.  Certain  poisons  dissolve 
hemoglobin  easily,  forming  methemoglobin  without 
material  change  of  the  stroma,  as,  for  instance,  sodium 
nitrit,  potassium  permanganat,  pyrogallic  acid,  anti- 
febrin. Others  again,  especially  the  chlorin  salts  and 
arseniated  hydrogen,  preferably  destroy  the  red  blood 
corpuscles,  though  not  always  immediately.  The  dis- 
solution of  the  erythrocytes  with  the  transfusion  of  the 
lecithin  into  the  plasma,  causes  a  splitting  of  the  lecithin 


DYSPNCEA   AND    CYANOSIS  157 

and  the  formation  of  glycerophosphoric  acid  which 
acidulates  the  blood.  In  other  cases,  there  is  a  toxic 
formation  of  acids  by  inhibition  of  the  oxydation  of 
the  acids  due  to  the  albuminoid  metamorphosis  of  the 
tissues,  as  lactic  acid,  the  presence  of  which  in  the 
blood  in  a  case  of  arsenical  poisoning  was  demon- 
strated by  H.  Meyer,  Both  the  increase  of  the  acidity  of 
the  blood  and  the  formation  of  toxic  acids  may  in  such 
cases  of  poisoning  play  a  role  in  the  production  of 
dyspnoea,  inasmuch  as  in  acid  intoxication  the  tissues 
lose  their  ability  of  absorbing  the  oxygen  which  the 
blood  offers  them. 

ANTIPYRIN^    BENZOL   DERIVATIVES ACETANILID 

Cyanosis  after  the  use  of  antipyrin  has  frequently 
been  observed.  Bamberger  reported  the  case  of  a 
lady  who,  each  time  after  the  administration  of  fifteen 
grains  of  antipyrin  for  the  relief  of  migraine,  became 
blue  without  any  other  symptom.  I  personally  ob- 
served a  case  of  hysteria  in  which  there  was  consid- 
erable cyanosis  of  the  skin  after  the  administration  of 
ten  powders  of  seven  and  a  half  grains  each  of  anti- 
pyrin. The  face  was  especially  cyanotic  and  the  pulse 
was  accelerated,  with  a  condition  bordering  on  collapse 
and  with  hysterical  contractions  of  the  extremities. 
The  treatment  with  antipyretics — antipyrin,  lactophe- 
nin,  etc. — to  cure  febrile  conditions  may  be  followed 
by  cyanosis,  which,  however,  does  not  have  the  dis- 
quieting significancej  especially  in  typhoid,  which 
accompanies  other  disturbances  of  the  circulation. 


158      DISORDERS   OF   RESPIRATION    AND   CIRCULATION 

In  anilin  poisoning  as  well  as  in  poisoning  with  ben- 
zol derivatives,  especially  acetanilid.  there  is  in  addi- 
tion to  the  vertigo,  headache,  dyspnoea,  muscular  weak- 
ness with  fibrillary  contractions  and  somnolence,  also 
cyanosis  as  the  most  prominent  symptom.  It  is 
frequently  accompanied  by  hematuria,  strangur}^  and 
oftentimes  by  icterus.  Poisoning  with  nitro-com- 
pounds  of  the  aromatic  series  (nitrobenzol,  dini- 
trobenzol,  nitrotoluol),  which  are  employed  in  blasting 
operations,  produces  considerable  cyanosis  which  some- 
times appears  even  before  the  other  symptoms  of  poi- 
soning. The  blood  is  of  a  chocolate  color,  but  does 
not  always  contain  methemoglobin,  according  to 
the  experiments  of  Huber  and  Haldane,  but  rather,  as 
it  would  seem,  a  nitro-compound  of  hemoglobin,  which 
is  also  incapable  of  respiration  (Dehio:  anilin  black). 
In  workmen  employed  in  rectifying  petroleum,  Eulen- 
berg  frequently  observed  cyanosis  of  the  lips  and  a 
bluish  complexion. 

NITROGLYCERIN^  AMYL  NITRIT  AND  CARBOLIC  ACID 

Nitroglycerin  and  also  amyl  nitrit  poisoning  cause 
considerable  cyanosis,  severe  headache,  dyspnoea  and 
muscular  debility,  and  the  cyanosis  outlasts  all  the 
other  manifestations  even  in  favorable  cases.  In  the 
three  fatal  cases  of  nitrogtycerin  poisoning  observed  by 
Nystrom,  death  ensued,  without  convulsions,  in  coma 
after  considerable  dyspnoea  and  cyanosis.  Carbolic 
acid  poisoning  also  causes  dyspnoeic  breathing  with 
cold,  cyanotic  skin  as  a  prominent  symptom,  in  addi- 


DYSPNCEA    AND    CYANOSIS  1 59 

tlon  to  the  well-known  corrosive  effect  on  the  esopha- 
gus and  the  stomach,  the  dark  olive-colored  urine  and 
the  loss  of  consciousness. 

ARSENIATED    HYDROGEN    AND    POTASSIUM     CHLORAT 

In  poisoning  with  arseniated  hydrogen  and  potas- 
sium chlorat,  cyanosis  and  dyspnoea  form  a  prominent 
symptom  as  a  consequence  of  the  serious  injury  to  the 
blood,  aside  from  the  other  well-known  manifestations 
of  intoxication.  A  not  uninteresting  observation  in 
these  cases  is  the  appearance  of  nuclear  erythrocytes  in 
the  blood,  occasioned  by  toxic  irritation  of  the  mar- 
row. A  working  man,  observed  by  me,  who  had  been 
employed  in  filling  a  balloon,  inhaled  arseniated  hydro- 
gen and  developed  sleepiness  and  considerable  cyanosis. 
The  blood  contained  large  quantities  of  nuclear  ery- 
throcytes without  any  eosinophile  cells  and  without 
myelocytes,  a  fact  which  under  certain  circumstances 
may  have  a  diagnostic  significance  as  against  other  in- 
toxications, especially  cholera. 

Another  factor  deserves  mention  in  these  cases  of 
poisoning.  The  destruction  of  the  red  blood  corpus- 
cles, which  takes  place  as  methemoglobin  is  being 
formed,  may  lead  to  obstruction  of  the  vessels  in  the 
internal  organs,  especially  the  lungs,  by  the  debris  of 
the  destroyed  erythrocytes  and  in  this  way  cause  dis- 
turbances of  the  circulation  and  respiration.  A  sim- 
ilar process  occurs  in  burns  of  the  skin,  in  which  there 
are  cyanosis,  dyspnoea,  coma  and  low  temperature  with 
lessened  blood  pressure,  so  that  not  only  the  toxic  ef- 


l6o      DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

feet  through  resorption  of  the  poisons  formed  at  the 
injured  places  should  be  considered,  but  also  multiple 
thrombi  due  to  the  debris  of  destroyed  red  blood  cor- 
puscles. 

NITRITS SODIUM  AND  POTASSIUM 

The  nitrits  have  a  special  significance  in  the  patho- 
genesis of  cyanosis.  It  is  a  well-known  fact  that  both 
sodium  and  potassium  nitrit  belong  to  the  poisons 
which  form  methemoglobin.  The  nitrats  have  no 
such  effect,  but  it  is  possible  that  they  are  changed  into 
nitrits  in  the  organism.  Since  the  bacilli  of  putrefac- 
tion and  pathogenic  fungi,  as  anthrax  bacilli,  may  re- 
duce nitrats  to  nitrits,  a  similar  change  may  well  take 
place  in  the  intestinal  canal  and  perhaps  also  in  the 
blood.  Nitrits  cause  cyanosis  by  the  formation  of 
methemoglobin,  which  paralyzes  the  muscles  of  the 
blood  vessels  and  reduces  the  blood  pressure.  Even 
after  medicinal  doses  of  sodium  nitrit  (six  grains) 
cyanosis  has  been  observed. 

In  1893  Emmerich  and  Tsuboi  tried  to  explain 
Asiatic  cholera  as  a  nitrit  poisoning,  based  upon  the 
discovery  of  methemoglobin  in  the  bodies  of  guinea 
pigs  which  had  died  of  cholera,  and  upon  similar  find- 
ings in  the  blood  of  test  animals,  poisoned  with  sodium 
nitrit.  It  had  been  known  for  a  considerable  time 
that  cholera  bacilli  are  capable  of  oxydizing  ammonia 
from  its  combinations  into  nitrous  acid  and  that  they 
are  distinguished  from  many  other  bacteria  in  being 
able  to  change  nitrats  into  nitrits.     During  the  chol- 


DYSPNCEA   AND   CYANOSIS  l6l 

era  epidemic  in  the  autumn  of  1892  I  paid  special  at- 
tention to  the  nitrifying  ability  of  the  cholera  bacillus, 
examining  not  only  the  cultures  of  the  cholera  bacillus, 
but  also  the  feces  of  patients.  The  gelatine  cultures 
of  the  cholera  bacillus  obtained  from  the  stool  of  the 
first  fatal  case  in  Vienna,  were  stained  red  (nitrous 
acid)  by  both  sulfanilic  acid  and  naphthylamin,  while 
with  diphenylamin  they  promptly  reacted  to  nitrats. 
On  the  other  hand,  I  have  not  succeeded  in  demonstrat- 
ing either  nitric  or  nitrous  acid  in  the  feces  of  chol- 
era patients,  dead  or  alive,  after  they  have  been  acid- 
ulated with  sulphuric  acid.  Examinations  of  the  blood 
and  urine  of  cholera  patients  for  the  presence  of  ni- 
trits  have  not,  to  my  knowledge,  been  made,  while 
personally  I  did  not  have  an  opportunity  of  making 
them.  Besides,  the  picture  of  nitrit  poisoning  in  the 
human  being  does  not  correspond  at  all  with  that  of 
cholera. 

The  usual  manifestations  in  nitrit  poisoning  consist 
of  headache,  great  weakness,  nausea  and  cyanosis. 
Isolated  cases  of  poisoning  with  large  doses  of  nitrit 
have  been  known,  where  there  were  grave  manifesta- 
tions of  collapse  and  simultaneously  vomiting  and 
diarrhea.  This  may  easily  happen  if  part  of  the  in- 
gested nitrits  has  already  undergone  chemical  decom- 
position in  the  stomach,  and  liberated  nitrous  acid. 
True  gastro-enteritis  with  uncontrollable  vomiting  and 
ricewater  stools  has  not  been  observed  in  these  cases. 
Although  at  the  present  time  nobody  harbors  the  idea 
of  connecting  single  symptoms  of  cholera  intoxication 


1 62      DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

as  cyanosis  with  nitrits,  yet  in  recent  times  intestinal 
autointoxication  has  been  observed  in  which  nitrits 
probably  formed  in  the  intestines  under  the  influence 
of  nitrifying  bacteria,  seemed  to  have  played  a  part. 

Hymans  van  den  Bergh  and  Grutterink  found  in 
many  cases  of  enterogenous  cyanosis  from  methemo- 
globinemia, nitrits  showing  Griess's  reaction  in  the 
blood.  With  strict  milk-diet  the  cyanosis  disappeared 
after  twenty-four  hours,  but  reappeared  upon  the  re- 
sumption of  a  mixed  diet.  Gibson  and  Douglas  ob- 
served in  the  blood  of  a  cyanotic  woman  of  thirty- 
six,  complaining  of  vertigo,  headache  and  diarrhea, 
methemoglobin  and  nitrits,  the  latter  also  in  the  sa- 
liva. The  bacteriological  examination  of  the  blood 
revealed  the  presence  of  a  bacterium  of  the  colon  group, 
to  which  the  formation  of  nitrits  and  methemoglobin 
was  attributed. 

NITROUS  ACID^   PRUSSIC  ACID 

In  poisoning  by  the  ingestion  of  nitrous  acid  there 
are  corrosive  effects,  asthmatic  attacks  of  suffocation 
and  asphyxia  with  severe  cyanosis.  On  the  other  hand 
it  has  been  observed  that  the  intoxication  by  this  acid 
produced  almost  the  identical  symptoms  as  did  the 
poisoning  by  ammonia. 

Poisoning  with  prussic  acid  leads  rapidly  to  death, 
either  by  instantaneous  general  paralysis  or  by  stupor, 
paralysis  of  the  heart  and  convulsions,  accompanied  by 
an  initial  cry  as  in  epileptic  seizures.  In  chronic  in- 
toxications with  substances  which  yield  prussic  acid, 


DYSPNCEA   AND    CYANOSIS  163 

as  bitter  almonds,  there  is  in  addition  to  acceleration 
of  the  respiration  and  oppression  of  the  chest,  dilata- 
tion of  the  pupils,  salivation,  coldness  of  the  extremi- 
ties and  cyanosis  of  the  mucous  membranes,  the  face 
and  the  entire  body. 

Robertson  and  Winne  reported  seven  cases  of  prus- 
sic  acid  poisoning  after  the  ingestion  of  the  beans  of 
the  faseolus  lunatus.  Four  of  them  terminated  fatally 
within  eleven  hours  and  death  ensued  with  severe  dysr 
pnoea  and  convulsions.  From  first  to  last  the  picture 
was  the  result  of  a  deep  disturbance  of  the  function  of 
respiration. 

Dyspnoea  in  prussic  acid  poisoning  does  not  depend 
upon  the  formation  of  cyanmethemoglobin,  which 
it  produced  only  in  experiments  in  a  solution  of 
methemoglobin.  Numerous  experiments  have  dem- 
onstrated that  the  cyanosis  is  not  caused  by  the  blood 
being  unable  to  give  up  oxygen,  as  is  the  effect  in 
poisoning  with  carbonmonoxidhemoglobin,  but  by 
the  fact  that  the  tissues,  especially  the  ganglionic  cells 
of  the  center  for  respiration,  lose  their  power  of  ab- 
sorbing the  oxygen,  which  is  abundantly  offered  to 
them.  The  deficiency  of  oxygen  resulting  therefrom 
leads  to  a  most  violent  excitation  of  the  center  for  res- 
piration which  rapidly  passes  into  paralysis.  On  ac- 
count of  its  strong  effect  upon  the  center  for  respira- 
tion prussic  acid  has  been  proposed  as  an  antidote  to 
chloroform  poisoning,  but  so  far  it  has  been  employed 
only  in  veterinary  practice.  Horday  used  it  with  good 
success  on  a  large  number  of  dogs. 


164      DISORDERS  OF  RESPIRATION   AND  CIRCULATION 
SULFURETTED   HYDROGEN 

The  effect  of  sulfuretted  hydrogen  is  similar  to  that 
of  prussic  acid.  In  light  cases  of  poisoning  there  is 
only  iritation  of  the  conjunctiva  and  nasal  mucous 
membrane,  but  at  times  also  vertigo,  nausea  and  se- 
vere dyspnoea.  If  large  quantities  of  the  poisonous 
gas  invade  the  respiratory  tract,  as  may  happen  to 
workmen  in  sewers  and  drains,  respiration  is  at  once 
accelerated,  soon  becomes  labored  and  highly  dys- 
pnoeic,  the  pulse  weak,  the  skin  cold  and  cyanotic,  and 
the  abdomen  exceedingly  distended.  There  may  be 
convulsions  and  coma,  followed  by  death  from  edema 
of  the  lungs  and  cessation  of  respiration.  The  as- 
phyctic manifestations  may  subside  even  in  grave  cases 
and  recovery  takes  place,  different  from  carbonmonoxid 
poisoning.  This  is  explained  by  the  rapid  exhalation 
of  the  poison  from  the  lungs,  and  is  corroborated  by 
the  fact  that  the  expired  air  in  man  and  animals,  poi- 
soned with  sulfuretted  hydrogen,  blackens  a  sheet  of 
acetate  of  lead  paper  held  before  the  mouth.  It  also 
agrees  with  the  fact  that  in  intravenous  injections, 
sulfuretted  hydrogen  is  not  absorbed  by  the  arterial 
blood.  This  rapid  elimination  of  the  poison  explains 
too  why  the  intoxications  which  happen  to  chemists, 
and  the  autointoxications  due  to  the  absorption  of  the 
intestinal  sulfuretted  hydrogen  into  the  circulation,  do 
not  usually  take  a  dangerous  course.  In  the  rectal  ap- 
plication of  sulfuretted  hydrogen,  recommended  by 
Altmann  for  the  treatment  of  tuberculosis,  no  toxic 


DYSPNOEA   AXD    CYANOSIS  1 65 

S}'mptoms — dyspncea  or  cyanosis — were  obser\-ed.  On 
the  other  hand,  Hymans  van  den  Bergh  and  Gutter- 
ink  have  reported  cases  of  enterogenic  cyanosis  with 
obstinate  constipation,  in  which  the  blood  is  said  to  have 
contained  sulfhemoglobin,  which  disappeared  after 
evacuation  of  the  intestine.  This  result  is  almost  un- 
explainable,  since  all  attempts  to  demonstrate  during 
life  sulfhemoglobin  in  the  blood,  even  in  grave  and 
fatal  intoxications  with  sulfuretted  hydrogen,  have 
been  unsuccessful. 

BOTULISM,     TETAXUS     TOXIX,    POISOXOUS     FISH 

Botulism,  that  is,  poisoning  by  decomposed  sau- 
sages and  albuminous  food  (both  meat  and  vegetable 
preser\^es),  resembles  the  symptom-complex  of  atro- 
pin  poisoning,  in  so  far  as  the  intoxication  with  the 
toxin  of  botulism,  but  not  when  there  is  an  infection 
with  the  bacterium  coli  and  Gaertner's  bacillus.  Among 
the  symptoms  are  dyspnoea  with  precordial  anx- 
iety, anno}-ing  and  often  spasmodic  cough,  dysphagia, 
glossoplegia,  dryness  of  the  mouth,  paresis  of  accom- 
modation, paralysis  of  the  ocular  muscles,  ptosis  with 
cardiac  weakness,  cold,  pale  skin,  and  lividity  of  the 
mucous  membranes.  These  bulbar  symptoms  result 
from  the  combination  of  the  toxin  of  botulism  with  the 
ganglionic  cells  of  the  bulbar  nuclei. 

A  similar  elective  affinity  for  the  nen^ous  system, 
especially  for  the  ganglionic  cells  of  the  anterior  cor- 
nua  and  of  the  bulbar  nuclei,  is  characteristic  of 
tetanus  toxin.     The  symptoms,  which  appear  at  the 


1 66      DISORDERS  OF  RESPIRATION  AND   CIRCULATION 

climax  of  an  attack,  are  dyspnoea  with  fear,  livid  skin, 
frothing  at  the  mouth  due  to  spasm  of  the  muscles  of 
the  glottis,  tongue  and  respiration. 

Intoxications  from  eating  poisonous  fish  (unsalted 
sturgeon)  also  belong  to  this  group.  These  fish  con- 
tain a  ptomain,  with  an  action  similar  to  atropin,  which 
is  destroyed  by  boiling  and  is  thus  different  from  the 
poison  by  the  Japanese  tetroden,  which  is  not  de- 
stroyed by  heat.  The  symptoms  after  the  ingestion  of 
the  various  species,  sphyrena,  coryphen  and  scomber, 
are  a  red  or  violet  complexion,  often  considerable 
edema,  especially  of  the  lips  and  eyelids,  difficulty  in 
breathing  of  an  asthmatic  nature,  occasionally  acute 
coryza  with  sneezing,  lachrymation  and  spastic  cough, 
and  resemble  closely  urticaria  of  the  skin  and  mucous 
membranes,  after  partaking  of  strawberries,  lobster, 
etc. 

INSECT  STINGS,  SNAKE  BITES 

Insect  stings  may  occasion  general  symptoms  with 
fainting,  cardiac  weakness,  difficulty  in  breathing, 
cyanosis  of  the  lips,  coldness  of  the  extremities  and 
fatal  collapse,  especially  when  the  sting  empties  its 
poison  directly  into  a  blood  vessel.  Stings  in  the 
mouth  or  fauces  from  eating  fruit  in  which  bees  or 
wasps  are  hidden,  become  dangerous  on  account  of  the 
edema  of  the  glottis  they  may  produce  (Bollinger). 
Stings  by  hornets  {vesta  crabro),  whose  poison  is 
said  to  immunize  against  viper  poison  according  to 
experiments  made  by  Physalix,  may  be  followed  by 
severe  general  symptoms,  with  dyspnoea,  sensation  of 


DYSPNOEA   AND   CYANOSIS  idj 

oppression  and  collapse.     The  same  is  true  of  scorpion 
stings. 

Finally,  rapidly  appearing  dyspnoea  with  slow  and 
irregular  respiration,  facies  hippocratica  with  coma 
and  paralysis,  cyanosis  and  scorbutus-like  hemorrhages 
into  all  tissues  of  the  body,  without  injury  of  the  ves- 
sels consequent  upon  hemolysis,  are  symptoms  of  the 
poisoning  from  snakebites. 

BERI-BERI,  ANESTHETIC  LEPROSY 

Beri-beri,  a  disease  occurring  in  Japan  and  China, 
is  regarded  by  some  as  an  intoxication  due  to  decom- 
posed vegetable  or  animal  matter,  and  by  others  as  an 
infectious  disease.  It  frequently  occurs  with  dyspncea 
and  weak  cardiac  function,  paralysis  of  the  lower  ex- 
tremities, atrophy  of  the  muscles,  similar  to  alcoholic 
neuritis  and  myxedema  of  the  skin.  The  dyspncea  is 
occasioned  partly  by  neuritic  changes  in  the  pneumo- 
gastrie  and  phrenic  nerves,  in  part  by  fatty  degenera- 
tion of  the  cardiac  muscle,  especially  in  those  forms 
running  a  rapid  course  and  leading  to  death  through 
cardiac  inefficiency  with  cyanosis. 

In  anesthetic  leprosy,  bulbar  symptoms  have  to  my 
knowledge  never  been  described,  although  neuritic 
processes  belong  to  the  characteristic  findings  due  to 
leprous  infiltration  of  the  peripheral  nerves,  the  ulnar 
and  major  auricular  nerves.  In  lepra  tuberosa,  as 
already  mentioned,  localization  of  the  disease  in  the 
larynx,  trachea  or  even  lungs,  may  cause  severe  dys- 
pnoea with  stenotic  symptoms.     The  susceptibility  of 


1 68      DISORDERS   OF  RESPIRATION   AND   CIRCULATION 

leprous  patients  to  iodin  preparations  is  well  known. 
Frequently  they  react  to  comparatively  small  doses  of 
potassium  iodid  in  a  way  similar  to  tuberculin,  caus- 
ing hyperemia  and  edema  of  the  affected  parts.  In 
laryngeal  lepra  there  may  be  stenosis  from  edema  of 
the  glottis  after  the  administration  of  potassium  iodid. 


VIII 

DYSPNCEA  AND  CYANOSIS  IN  GENERAL 
DISEASES 

BRIGHT^S  DISEASE 

Dyspnoea  and  cyanosis  occur  in  subacute  or  chronic 
affections  of  various  organs  when  secondary  changes 
in  the  circulation  and  respiration  are  added.  Bright's 
disease,  in  which  dyspnoea  may  be  due  to  various 
causes,  belongs  especially  in  this  class. 

Renal  asthma  oftentimes  occurs  acutely  and  in 
paroxysms  without  demonstrable  bronchial  or  pul- 
monary affection.  In  other  cases  there  is  a  transitory 
bronchial  catarrh  with  rales,  which  change  their  site 
and  disappear  after  the  paroxysm.  Besides  these 
mobile  and  transitory  edemas  there  is  also  a  genuine 
pulmonary  edema  with  characteristic  sputa.  In  the 
final  phase,  the  dyspnoea  is  permanent  with  nightly 
exacerbations  as  in  cardiac  asthma,  except  that  hemop- 
tysis and  hemorrhagic  infarcts  are  rare.  The  hem- 
orrhages from  the  lungs  and  the  bronchial  mucous 
membranes,  if  they  do  occur  at  all,  are  as  a  rule  the 
expression  of  a  hemorrhagic  diathesis. 

Cyanosis  does  not  develop  even  though  the  functional 
energy  of  the  left  ventricle  be  weakened,  provided  that 
the  anemia,  which  in  nephritic  cases  sometimes  reaches 
a  hi^h  degree,  is  marked. 

169 


I/O      DISORDERS   OF  RESPIRATION  AND  CIRCULATION 
CHRONIC    NEPHRITIS 

There  are,  however,  cases  of  chronic  nephritis  in 
which  the  blood  has  suffered  little  in  spite  of  the  chro- 
nicity  of  the  affection.  In  these  cases  the  clinical  signs 
may  begin  with  gallop  rhythm,  cyanosis,  congested 
lung,  enlarged  liver,  sometimes  with  reduced  diuresis  if 
previously  there  was  polyuria,  so  that  the  differential 
diagnosis  as  to  the  presence  of  cor  renale  or  ren 
cardiaciis  may  cause  difficulty.  The  differential  diag- 
nosis may  depend  upon  the  variations  in  the  excretion 
of  nitrogen,  especially  of  urea,  retention  changing  with 
considerable  excretion,  diminution  of  phosphoric  acid 
as  a  rule,  especially  that  form  combined  with  alkaline 
earths,  upon  the  normal  relation  of  sulphuric  acid  to 
nitrogen  in  conjunction  with  normal  or  reduced  diure- 
sis, increased  concentration  of  the  blood,  especially  in 
contracted  kidney,  and  other  clinical  symptoms  of  pri- 
mary  renal   affection,   such  as  retinitis. 

CONTRACTED  KIDNEY^  CYSTIC  KIDNEY 

Gallop  rhythm  is  a  frequent  occurrence  in  genuine 
contracted  kidney,  while  arrhythmia  is  rare.  In 
arteriosclerotic  contracted  kidney,  however,  cardiac 
arrhythmia  is  frequent  in  consequence  of  the  myo- 
carditic  changes  of  the  heart — and  there  may  be  hard 
pulse  with  high  blood  pressure  during  the  dyspnceic 
paroxysms  in  spite  of  inefficiency  of  the  ventricle.  It 
should  also  be  remarked  that  congenital  cystic  kid- 
neys, imless  they  are  complicated  by  nephritis,  may  be 
entirely  free  from  increased  blood  pressure,  even  in 


DYSPNOEA   AND   CYANOSIS  I7I 

manifest  uremia,  forming  a  striking-  contrast  to  the 
uremia  of  contracted  kidney.  Lowered  or  not  ma- 
terially increased  blood  pressure  in  the  presence  of 
uremic  manifestations  should  therefore  remind  us  of 
cystic  kidney  and  demands  a  careful  palpation  of  the 
renal  region.  If  cystic  kidney  is  kept  in  mind  as  a 
possible  cause  of  uremia,  it  will  not  be  difficult  to  es- 
tablish a  positive  diagnosis,  in  case  the  bilateral,  usually 
non-fluctuating,  nephritic  enlargement  can  be  felt, 
which  generally  makes  the  characteristic  impression  of 
a  bunch  of  grapes.  Cystic  kidneys  complicated  with 
chronic  nephritis  lead  to  hypertrophy  of  the  left  ven- 
tricle and  high  blood  pressure.  The  fact  of  uremia 
and  increased  blood  pressure  not  always  running  in 
parallel  lines  is  perhaps  of  theoretical  importance  in 
looking  upon  uremia  as  an  intoxication. 

RENAL  ASTHMA   VERSUS    CARDIAC   ASTHMA 

The  inefficiency  of  the  hypertrophic  left  ventricle 
in  the  course  of  latent  contracted  kidney  may  occur 
acutely,  and  not  infrequently  the  renal  asthma  is  the 
first  sypmtom  of  the  affection.  For  the  purpose  of 
differential  diagnosis  from  asthmatic  paroxysms  in 
primary  cardiac  affections,  it  should  be  noted  that  the 
urine  voided  during  the  paroxysm  is  albuminous,  light 
colored,  less  rich  in  coloring  matter,  and  larger  in 
quantity  than  in  cardiac  asthma.  In  the  latter  affec- 
tion the  urine  is  usually  dark,  concentrated,  contains 
urobilin,  has  a  high  specific  gravity  and  deposits 
abundant  sedimenfum  lateritium  after  the  asthmatic 


172      DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

attacks.  The  urine  in  nephritis  may  remain  light 
yellow  even  if  febrile  processes  develop  in  the  lungs 
or  pericardium.  The  urine  in  B right's  disease  does 
not  always  show  the  characteristics  of  febrile  urine, 
or  that  of  congestion^  in  spite  of  the  presence  of  stasis 
and  fever. 

LATENT   NEPHRITIS 

In  latent  nephritis  a  simple  acute  catarrh  of  the 
respiratory  tract  may  sometimes  suddenly  and  with- 
out warning  present  the  clinical  picture  of  severe 
dyspnoea  and  general  dropsy  with  numerous  rales, 
causing  death  from  a  complicating  edema  of  the  lungs. 
This  is  explainable  by  the  fact  that  in  nephritis  an 
irritation  of  a  tissue  is  frequently  provocative  of 
edema.  Just  as  a  simple  catarrhal  larjmgitis  may  pro- 
duce edema  of  the  larynx,  small  pneumonic  foci  may 
lead  to  edema  of  the  lungs.  In  the  same  way  sudden 
dyspncea,  cyanosis  and  coma  in  chronic  Bright's  dis- 
ease are  not  infrequently  semiotic  signs  of  commencing 
pneumonia  which  may  in  a  very  short  time  lead  to 
edema  of  the  lungs  and  death,  without  the  objective 
signs  of  pneumonia  being  clearly  demonstrable.  In 
such  cases  constant  elevation  of  temperature  may  be 
diagnostically  of  value  in  contrast  to  the  purely  toxic 
form  of  uremic  dyspnoea  and  of  uremic  coma,  in 
which  the  temperature  of  the  body  generally  falls,  pro- 
vided there  is  no  simultaneous  cerebral  hemorrhage, 
which  would,  after  originally  lowering  the  tempera- 
ture, cause  a  rapid  rise. 


DYSPNCEA   AND   CYANOSIS  173 

At  times  pulmonary  edema  may  occur  from  bodily 
overexertion,  mountain  climbing,  alcoholic  intoxica- 
tion, sexual  excesses,  use  of  certain  drugs,  as  opium, 
even  in  small  quantities,  also  from  acute  gastric  ca- 
tarrh in  consequence  of  sudden  weakness  of  the  left 
ventricle,  while  the  right  ventricle  still  functionates. 
In  these  cases  there  are  also  direct  clinical  signs  of 
disturbed  function  of  the  left  ventricle,  as  dilatation 
and  gallop  rhythm. 

HEMOPTYSIS   IN   CONTRACTED   KIDNEY 

In  cases  where  these  signs  on  the  part  of  the  ven- 
tricle are  absent,  and  yet  there  are  symptoms  of  stasis 
in  the  venous  and  pulmonary  systems  with  high  blood 
pressure,  the  cause  will  be  found  in  degeneration  of  the 
muscle  of  the  left  auricle.  Bamberger  in  his  lectures 
has  referred  the  hemoptysis,  which  sometimes  occurs 
as  the  first  warning  of  a  contracted  kidney,  to  a  hyper- 
emia of  the  lungs  from  dilatation  of  the  left  auricle. 
In  the  administration  of  digitalis  or  ergotin  to  remove 
these  symptoms,  caution  should  be  exercised.  On  ac- 
count of  the  abnormal  tension  of  the  aortic  system,  a 
cerebral  hemorrhage  may  easily  be  produced,  especially 
in  cases  of  B right's  disease  prone  to  such  a  result. 
The  diagnosis  of  dilatation  of  an  auricle  is  still  further 
confirmed,  if  during  prolonged  observation  cyanosis 
as  well  as  the  other  manifestations  of  congestion  in 
the  lungs  and  other  organs  increase,  while  the  ex- 
amination of  the  left  ventricle  does  not  reveal  any 
striking  changes;  neither  a  progressively  increasing 


174      DISORDERS  OF  RESPIRATION   AND  CIRCULATION 

dislocation  of  the  cardiac  impulse,  nor  in  a  functional 
respect,  a  decrease  of  the  arterial  tension.  The  forma- 
tion of  thrombi  in  the  right  auricle,  secondary  em- 
boli in  the  lung,  also  of  thrombi  in  the  dilated  left 
auricle  and  left  ventricle  may  impart  to  the  clinical 
picture  considerable  polymorphism  and  cause  great 
difficulty  in  the  diagnosis. 

CYANOSIS   OF   UREMIA 

Pronounced  cyanosis  of  an  edematous  face  with 
clonic  spasms  and  subsequent  coma,  after  preceding 
headache,  vomiting,  reduction  of  the  pulse  frequency, 
with  frequently  but  not  always  diminished  diuresis, 
belong,  as  is  well  known,  to  the  picture  of  an  uremic 
attack  and  are  occasioned  by  the  engorgement  of  the 
tissues  during  the  spasm.  The  cyanosis  of  the  face  oc- 
curs in  the  same  way  as  in  epilepsy.  The  paroxysmal 
dyspnoea  of  nephritis,  which  is  generally  designated  as 
uremic  dyspnoea,  occurs  with  or  without  cyanosis 
if  there  are  no  convulsions,  and  the  cyanosis  in  these 
cases  is  entirely  dependent  on  the  behavior  of  the 
heart.  In  uremic  dyspnoea  cyanosis  is  entirely  ab- 
sent, if  the  dyspnoea  is  occasioned  by  toxic  irritations  of 
the  bulbar  center  for  respiration  by  excrementitious 
urinary  substances. 

REDUCED  HEMOGLOBIN   IN   BLOOD 

According  to  Labbe  the  capillary  blood  contains 
0.5  to  1%  of  reduced  hemoglobin.  In  valvular  de- 
fects the  quantity  of  the  reduced  hemoglobin  increases 


DYSPNCEA  AND   CYANOSIS  175' 

to  2%,  especially  after  exertions,  in  disturbances  of 
compensation  up  to  3%,  5%,  and  at  times  even  7%, 
and  in  congenital  cardiac  defects  up  to  10%.  In 
uremic  dyspnoea  the  quantity  of  the  reduced  hemo- 
globin does  not  run  parallel  with  the  intensity  of  the 
dyspnoea.  In  three  cases  2%  were  found.  Labbe 
concludes  from  these  investigations  that  uremic  dys- 
pnoea is  of  toxic  origin,  while  cardiac  dyspnoea  is  rather 
to  be  attributed  to  obstruction  of  the  circulation. 

DIABETES 

Since  Kussmaul's  classic  presentation,  the  dyspnoea 
which  ushers  in  coma  diabeticum  is  looked  upon  as 
an  integral  symptom  of  the  pathological  picture.  This 
form  of  coma,  characterized  by  an  accelerated,  regu- 
lar, strongly  dyspnoeic  and  deep  respiration,  is  desig- 
nated as  coma  diabeticum.  In  true  diabetic  coma 
cyanosis  is  absent  in  spite  of  considerable  dyspnoea,  so 
that  the  absence  of  cyanosis  in  the  presence  of  inspira- 
tory dyspnoea  without  orthopnoea  is  a  direct  reminder 
of  diabetes.  Diabetic  dyspnoea  is  regarded  as  an  acid  in- 
toxication on  account  of  the  abundant  excretion  of  ace- 
tone, di-acetic  acid  and  B-oxybutyric  acid.  Through 
the  acidulation  of  the  blood  a  large  part  of  the  alkali 
in  the  blood  is  neutralized.  Since  the  alkali  of  the  blood 
is  the  important  element  which  chemically  binds  the 
carbon  dioxid,  the  decrease  of  blood  alkalinity  to- 
gether with  the  reduction  of  the  carbon  dioxid  capacity 
of  the  blood  in  diabetes  is  intelligible.  An  increase  in 
the  venosity  of  the  blood  therefore  does  not  take  place 


176      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

in  diabetic  acid-dyspnoea.  In  this  way  the  absence  of 
cyanosis  m  pure  cases  of  diabetic  coma,  not  compH- 
cated  by  pulmonary  and  cardiac  affections,  is  explained. 
In  contrast  to  diabetic  coma,  which  is  introduced 
and  characterized  by  dyspnoea,  there  are  also  cases  of 
fatal  coma  in  diabetes  in  which  Kussmaul's  dyspnoea 
is  absent.  These  cases  of  non-dyspnoeic  coma  in  dia- 
betes have  been  described  by  Lossen  (of  Lichtheim's 
Clinic  in  Konigsberg)  and  do  not  seem  to  stand  in  the 
same  relation  to  the  acidosis  of  diabetes,  as  effect  to 
cause.  Even  those  forms  of  diabetic  coma  where  the 
urine  and  blood  analysis  point  to  an  acid  intoxication, 
do  not  in  all  cases  present  the  typical  picture  of  Kuss- 
maul's respiration.  There  are  cases  in  which  there 
is  dyspnoea  without  deepening  of  the  respiration,  but 
with  disturbances  of  the  respiratory  rhythm,  as 
Cheyne-Stokes'  respiration,  and  again  cases  where 
there  are  epileptiform  spasms  without  real  dyspnoea 
as  an  expression  of  the  serious  damage  done  to  the 
central  nervous  system  by  the  abnormal  metabolic  pro- 
ducts in  diabetes. 

CYANOSIS  IN  DIABETES 

Cyanosis,  as  mentioned,  is  absent  in  diabetic  coma, 
but  in  the  acute  exacerbations  of  diabetes  it  may  ap- 
pear from  complications  w^ith  organic  affections  of  the 
respiration  and  circulation.  There  are  some  cases  of 
chronic  diabetes  with  a  slight  cyanotic  reddening  of 
the  face,  especially  of  the  ears  and  nose,  so  that  an 
impression  is  created  that  the  patient  is  a  alcoholic 
with  a  weak  heart.     These  bluish  discolorations  are 


DYSPNCEA   AND   CYANOSIS  177 

observed  both  in  obese  and  in  lean  diabetic  patients, 
affected  with  afebrile  tuberculosis.  Therefore,  in  cya- 
notic patients,  both  obese  and  with  afebrile  tuberculo- 
sis, the  urine  should  be  examined  for  sugar,  in  order 
not  to  overlook  the  primary  affection.  It  was  just 
this  manifestation  and  the  absence  of  night  sweats 
that  caused  me  to  diagnosticate  diabetes  mellitus  as 
the  primary  complaint  in  a  phthisical  patient  who  had 
been  sent  by  his  physician  to  Meran  to  take  a  grape 
cure. 

Of  a  totally  different  nature  are  those  forms  of  gly- 
cosuria in  which  in  addition  to  an  acute  dilatation  of 
the  heart  cyanosis  appears  with  grave  and  sometimes 
fatal  forms  of  tachycardia.  Both  the  glycosuria  and 
tachycardia  should  be  regarded  as  bulbar  symptoms. 
In  especially  complicated  cases  the  interpretation  of 
the  glycosuria  may  be  facilitated  by  an  investigation 
of  the  metabolism,  as  the  latter  in  all  genuine  forms 
discloses  an  increased  secretion  of  organic  and  inor- 
ganic urinary  substances  corresponding  with  the  dia- 
betic autophagia. 

HYDROPHOBIA 

Dyspncea  associated  with  precordial  fear,  with  fre- 
quent sighing  and  unusually  deep  inspiration,  with  a 
sensation  of  constriction  in  the  throat  is  an  early 
symptom  of  hydrophobia.  In  its  further  course  the 
dyspncea  increases  until  it  reaches  a  true  respiratory 
spasm,  and  is  accompanied  by  an  extreme  hyperes- 
thesia, which  affects  nearly  all  the  nerves,  especially 
the  pneumogastric,  phrenic,  glossopharyngeal  and  ac- 


178      DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

cessorius.  Hydrophobia  and  aerophobia  (fear  of 
water,  or  of  the  slightest  draught  of  air),  even  gen- 
eral convulsions  at  the  sight  of  water  and  of  a  crowd 
of  people,  dysphagia,  etc.,  are  only  part  manifestations 
of  the  hyperesthesia  and  increased  reflex  excitability, 
which  is  an  expression  of  the  profound  damage  to  the 
nervous  system.  There  is  a  striking  contrast  between 
the  cyanosis  and  the  extreme  pallor  of  the  skin,  es- 
pecially of  the  face,  which  assumes  a  livid  cyanotic 
color  only  during  the  convulsive  attacks  which  are 
similar  to  those  occurring  in  tetanus. 

In  the  paralytic  stage,  which  is  characterized  by 
decrease  of  the  dyspnoea  and  of  the  reflex  excitability, 
by  accelerated  and  stertorous  respiration  and  increas- 
ing cardiac  weakness,  with  small  and  exceedingly 
rapid  pulse;  disturbance  of  the  circulation  may  cause 
cyanosis  as  a  premortal  sign  that  may  persist  until 
death.  Death  ensues  either  under  asphyctic  convul- 
sions or  in  quiet  coma.  The  dyspnoea  of  rabies  is  of 
bulbo-medullary  origin  and  its  characteristic  is  the  ab- 
sence of  cyanosis  in  the  stage  of  the  excitement,  just 
as  is  the  acid  dyspnoea  of  diabetes.  In  the  course  of 
hydrophobia  intense  acetonuria,  together  with  dys- 
pnoea, has  been  noted  from  the  very  first  in  my 
patients.  This  symptom  may  have  a  diagnostic  signi- 
ficance in  contradistinction  to  hysterical  hydrophobia. 
Then  too  acetonuria  is  of  special  theoretical  interest 
in  an  affection  characterized  by  considerable  excita- 
tion with  complete  consciousness,  in  which  coma  occurs 
only  as  a  terminal  manifestation,  because  acetonuria 


DYSPNCEA!  AND   CYANOSIS  179 

by  way  of  contrast  always  accompanies  the  comatose 
stage  of  diabetes.  A  remarkable  fact  is  the  resistance 
shown  by  patients  with  hydrophobia  to  narcotics,  es- 
pecially to  preparations  of  opium.  In  one  of  my  pa- 
tients I  injected  morphin  up  to  seven  grains  without 
giving  the  slightest  relief.  Indeed,  it  appeared  to  me 
that  the  morphin  had  effected  an  increase  in  the  con- 
vulsions. This  power  of  resistance  in  this  affection  to 
the  specific  respiratory  poisons  recall  the  refractory 
behavior  of  cats  against  the  same  poison,  a  fact  with 
which  experimental  pathologists  are  thoroughly  fa- 
miliar. 

ANEMIA 

In  cases  of  grave  anemia,  either  true  or  post- 
hemorrhagic, there  are  no  material  changes  in  respi- 
ration unless  the  anemia  attains  an  extreme  degree. 
The  process  of  oxydation  shows  a  perfectly  normal 
behavior  in  the  consumption  of  oxygen  by  the  tissues, 
and  in  the  elimination  of  the  carbon  dioxid.  Highly 
anemic  patients  bear  impoverishment  of  the  blood 
from  defective  circulation  of  oxygen  very  well,  and 
avoid  everything  which  might  lead  to  a  greater  de- 
mand for  oxygen,  including  increased  activity  of  the 
respiratory  muscles.  Their  respiration  is  shallow  and 
superficial  and  they  do  not  become  dyspnoeic  during 
muscular  quiet.  When  the  demand  for  oxygen  is  in- 
creased, as  in  muscular  overexertions,  dancing,  car- 
rying heavy  loads,  etc.,  the  supply  of  oxygen  may 
become  insufficient.  This  insufficiency  is  shown  as 
polypnoea  with  the  subjective  sensation  of  air-hunger 


l80      DISOEDERS   OF  RESPIRATION  AND   CIRCULATION 

and  pronounced  dyspnoea,  the  purpose  of  which  is  to 
increase  the  aspiration  of  the  blood  into  the  thorax  and 
to  increase  the  circulation  and  aeration  of  the  lungs. 
As  muscular  activity  is  of  extreme  importance  in  the 
respirator}^  interchange  of  gases,  this  myogenic  dys- 
pnoea in  anemia  simply  means  a  repetition  of  the 
physiological  process  which  occurs  in  muscular  exer- 
tions and  disappears  in  muscular  quiet.  The  dyspnoea 
of  anemic  patients  disappears  with  rest  in  bed  and  is 
an  important  factor  in  the  therapy  of  chlorosis,  even 
in  those  forms  not  complicated  by  a  dilatation  of  the 
heart.  The  extra  work  demanded  of  the  thoracic 
muscles  can  be  estimated  by  the  dyspnoea  from  which 
chlorotic  girls  suffer  who  wear  tight  corsets  and  ex- 
perience no  further  trouble  upon  the  removal  of  the 
corsets.  All  these  forms  of  myogenic  dyspnoea  are 
the  result  of  irritation  of  the  center  of  respiration 
by  the  metabolic  products  of  active  muscles,  and  ane- 
mia is  a  condition  which  develops  this  physiological 
irritation  more  easily  and  rapidly. 

In  cases  of  anemia  accompanied  by  dilatation  of 
the  heart  and  involvement  of  the  muscular  substance, 
the  dyspnoea  is  due  to  these  complications,  and  the 
mechanism  is  the  same  as  that  of  the  cardiac  form  of 
dyspnoea. 

LEUKEMIA 

Dyspnoea  may  be  accentuated  in  leukemia  to  the 
most  violent,  asthmatic  paroxysms,  which  are  due, 
however,  less  to  the  changes  in  the  blood  than  to 
a  permanent  or  transitory  weakness  of  the  myocar- 


DYSPNCEA   AND   CYANOSIS  l8l 

dium.  Bamberger  has  emphasized  this  fact :  "  Neither 
the  changes  in  the  blood  of  themselves  nor  the  ob- 
struction to  respiration  by  an  enlarged  spleen  or  liver, 
nor  the  enlargement  of  the  bronchial  glands  are  a  suffi- 
cient explanation,  because  dyspncea  may  come  and  go 
without  any  change  in  these  conditions;  and,  besides, 
there  is  no  constant  relation  between  them."  In  doubt- 
ful cases  the  differential  diagnosis  as  to  whether  dys- 
pnoea is  of  myogenic,  hematogenic  or  cardiac  origin, 
may  be  established  by  enjoining  absolute  muscular 
rest  and  making  a  therapeutic  test  with  cardiac  reme- 
dies, as  digitalis,  strophanthus,  ether  and  camphor. 

Similar  to  leukemia,  subjective  dyspnoea,  especially 
in  exaggerated  muscular  exertions  with  negative  pul- 
monary findings,  frequently  associated  with  ver- 
tigo and  faint  feeling,  is  an  important  semiotic  sign 
of  those  forms  of  fatty  heart  which  are  at  times  ac- 
companied by  considerable  pallor  of  the  skin  and 
mucous  membranes.  In  cases  where  the  blood  exam- 
ination does  not  disclose  qualitative  changes,  we  find 
in  addition  to  the  dilatation  of  the  heart,  the  cardiac 
sounds  dull  and  soft,  especially  the  first  ventricular 
sound  and  the  blood  pressure  low  as  in  the  fatty  heart 
of  alcoholics.  In  other  cases,  where  the  blood  finding 
is  positive,  as  in  pernicious  anemia,  etc.,  there  are  gen- 
erally anemic  murmurs  over  the  heart  and  cervical 
vessels. 

ABSENCE  OF  CYANOSIS  IN  ANEMIA 

In  anemic  conditions  there  is  usually  no  cyanosis  in 
spite  of  the  dyspnoea,  because  the  blood  is  poor  in   red 


1 82      DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

blood  cells  and  hemoglobin.  Cyanosis  will  not  even 
appear  if  there  are  organic  affections  of  the  muscular 
substance  of  the  heart,  which  would  otherwise  lead  to 
cyanosis.  The  quantitative  changes  of  the  blood  are 
partly  decisive  for  the  absence  of  cyanosis,  also  the 
diminished  demand  for  oxygen  by  the  tissues,  and  in 
part  the  reduction  of  the  carbon  dioxid  in  consequence 
of  the  acidulation  of  the  blood.  The  appearance  of 
cyanosis,  if  only  as  a  livid  coloration  of  the  lips,  is 
therefore  of  increased  diagnostic  importance  in  cases 
of  grave  anemia,  because  it  indicates  considerable  de- 
generation especially  of  the  right  ventricle,  if  dilata- 
tion of  the  cardiac  cavities,  negative  findings  in  the 
lung,  and  absence  of  hemoglobinuria  are  demonstra- 
ble. Even  in  the  gravest  forms  of  pernicious  anemia, 
the  disturbance  of  circulation  does  not  always  corre- 
spond to  the  extent  of  the  anatomical  lesion  of  the 
cardiac  muscle.  The  autopsy  sometimes  discloses  fri- 
able muscular  substances,  while  during  life  there  were 
no  particular  indications  of  inefficiency  of  the  degen- 
erated muscle  and  vice  versa. 

Another  factor  may  be  of  importance  in  forming  an 
opinion  on  the  phenomena  under  discussion.  Lepine 
and  Bouloud  found  for  normal  blood  the  time  of  re- 
duction of  oxyhemoglobin  about  twenty  minutes.  In 
anemia  this  time  is  prolonged  up  to  about  an  hour. 
Prolonged  inhalation  of  chloroform  or  ether  also 
lengthened  the  time  of  reduction,  while  bacteriemia 
due  to  virulent  staphylococci  made  no  difference.  In 
dogs  which  had  been  rendered  artificially  anemic,  and 


DYSPNCEA   AND   CYANOSIS  183 

in  anemic  patients,  the  time  of  reduction  was  doubled 
and  sometimes  trebled.  Lepine  and  Bouloud  found  in 
the  gases  from  the  blood  of  persons  who  had  died  with 
grave  anemia  demonstrable  quantities  of  carbonmon- 
oxid,  and  consider  the  presence  of  carbonmonoxid- 
hemoglobin  one — if  not  the  only  cause,  for  the  retarded 
reduction  of  the  blood.  Should  these  findings  be  veri- 
fied, a  new  and  hitherto  neglected  factor,  aside  from 
deficiency  of  oxygen,  would  have  to  be  taken  into  ac- 
count to  explain  many  of  the  phenomena  and  the 
sequelae  of  grave  forms  of  anemia. 

POLYCYTHEMIA 

A  special  position  among  the  diseases  of  the  blood- 
forming  organs  is  occupied  by  affections  with  indefi- 
nite pathogenesis,  characterized  clinically  by  poly- 
cythemia with  enlarged  spleen  and  cyanosis;  dyspncea 
being  absent.  Cyanosis  of  the  mucous  membranes  and 
extremities  forms  the  chief  symptom  of  the  affection. 
It  does  not  depend  upon  the  presence  of  reduced 
hemoglobin,  nor  is  it  the  consequence  of  disturbances 
of  circulation,  but  originates  from  the  overfilling  of 
the  distended  vessels  with  blood  abnormally  rich  in 
hemoglobin.  The  color  of  the  patient  is  not  so  much 
a  blue  as  an  intense  purple.  The  blood  examination 
shows  a  surprising  increase  of  erythrocytes  up  to  over 
ten  millions  to  the  cubic  millimeter,  and  a  genuine 
plethora  with  increased  quantity  of  blood  which  ex- 
plains the  high  blood  pressure  and  the  tendency  to 
hemorrage  in  these  patients.    The  pathogenesis  of  the 


184      DISORDERS  OF  RESPIRATION  AND   CIRCULATION 

symptoms  in  these  patients  is  as  yet  unsettled,  but  it 
is  probable  that  the  nature  of  the  affection  consists  in  a 
primary  or  secondary  involvement  of  the  erythroblastic 
medullary  tissue  in  the  bone  marrow  leading  to  in- 
creased blood  formation,  in  a  similar  way  as  leukemia 
represents  a  hyperplastic  involvement  of  the  leuco- 
blastic  myeloid  tissue  with  increased  function. 

ASTHMA  DYSPEPTICUM 

The  asthma  which  is  occasioned  by  disturbances  of 
digestion  has  been  designated  dyspeptic  asthma.  Ac- 
cording to  communications  by  Henoch,  Silbermann, 
and  the  French  clinicians  (Barie),  this  is  not  a  me- 
chanical dilatation  of  the  stomach  by  gas,  nor  a 
mechanical  dyspnoea  from  an  elevated  position  of  the 
diaphragm,  but  a  grave  dyspnoea  which  in  specially 
predisposed  individuals  sometimes  occurs  immediately 
after  the  ingestion  of  food.  It  is  accompanied  by 
alarming  symptoms;  pallor  of  the  skin,  vertigo,  pre- 
cordial anxiety,  frequent,  superficial  and  at  times  re- 
tarded, deepened  respiration  without  obstruction  to  ex- 
piration, also  by  rapid  pulse,  dilatation  of  the  heart, 
sometimes  by  gallop  rhythm,  cyanosis  and  cold  ex- 
tremities. As  this  symptom-complex  is  acute,  the  idea 
suggests  itself  that  it  is  a  reflex  irritation  from  the 
stomach.  To  explain  the  mechanism  of  the  process, 
various  theories  have  been  advanced :  direct  paralysis 
of  the  inhibitory  fibers  of  the  pneumogastric  nerve  and 
a  vasomotor  spasm  of  the  arteries  of  the  general  circu- 
lation leading  to  temporary   inefficiency   of  the  left 


DYSPNCEA   AND   CYANOSIS  1 85 

heart.  In  other  cases,  the  right  instead  of  the  left 
ventricle  was  held  responsible  by  assuming  that  a 
spasm  of  the  pulmonary  vessels  induced  increased 
pressure  in  the  pulmonary  circulation  with  consequent 
inefficiency  of  the  right  ventricle.  In  a  similar  way 
the  paroxysmal  dyspnoea  of  gallstone  colics  has  been  ■ 
explained.  This  explanation  cannot  be  entirely  de- 
nied, since,  according  to  Strubell's  experiments,  the 
existence  of  vasomotor  processes  in  the  pulmonary 
circulation  is  very  probable,  Strubell,  by  paralysis 
of  the  pulse-retarding  fibers  of  the  pneumogastric  by 
strophanthin  and  by  subsequent  peripheral  irritation  of 
the  pneumogastric,  induced  a  fall  in  the  arterial  pres- 
sure, reduction  of  pressure  in  the  left  auricle,  slight 
increase  of  pressure  in  the  pulmonary  artery  and  con- 
siderable increase  in  the  right  auricle.  He  concludes 
therefrom  that  there  are  active  vasomotors  in  the  pul- 
monary vessels. 

Dyspeptic  asthma  presents  by  no  means  a  uniform 
symptom-complex.  Cases  in  which  there  are  latent 
cardiac  affections,  as  arteriosclerosis  or  fatty  heart, 
should,  of  course,  be  excluded,  as  they  do  not  properly 
belong  to  the  group  of  cardiac  asthma  which  is  caused 
by  disturbance  of  digestion  or  faulty  diet.  Nor  should 
cases  be  included  where  the  asthma  occurs  immediately 
after  excesses  in  drinking  and  smoking,  as,  aside  from 
the  fault  in  the  diet,  there  are  toxic  elements  in  the 
picture.  Grave  dyspeptic  asthma  after  acute  digestive 
disturbances,  especially  in  children  and  sometimes  ac- 
companied by  acetonuria,  should  not  be  designated  as 


1 86      DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

simple  cases  of  dyspeptic  asthma,  since  they  belong 
rather  to  the  group  of  toxic  or  toxic-infectious 
asthma,  occasioned  by  abnomial  fermentation  in  the 
intestines.  In  these  cases  the  signs  which  are  usually 
valid  for  the  diagnosis  of  intestinal  intoxication  will 
be  decisive,  as:  change  in  the  bacterial  flora  of  the 
intestine,  shown  by  the  prevalence  of  Gram-positive 
bacteria  coli,  which  are  usually  anerobic,  abnormal  in- 
crease of  indols  and  scatols,  furthermore  fermentative 
products  of  carbohydrates  in  the  stools,  the  sign  of 
intestinal  putrefaction  in  the  urine,  i.  e.,  the  increase 
of  ethereal  sulfuric  acid  in  proportion  to  sulfuric 
acid  and  nitrogen,  also  the  other  clinical  symptoms, 
meteorism,  borborygmi,  diarrhea  alternating  with 
obstipation,  foul-smelling  stools,  coated  tongue,  later 
vomiting,  and  finally  the  successful  treatment  by  cor- 
rected diet  and  disinfection  of  the  intestines. 

It  is  very  probable  that  those  attacks  of  dyspeptic 
asthma  which  occur  after  meals  in  persons  with  intact 
thoracic  organs,  affect  neurasthenic  or  hysterical  sub- 
jects, or  even  individuals  with  a  tendency  to  nervous 
asthma,  regardless  of  whether  there  is  hyperchlorhy- 
dria  or  achlorhydria.  Cases  have  been  described  in  the 
literature,  where  the  physiological  irritation  by  the 
gastric  juice  was  sufficient  to  cause  an  asthmatic 
paroxysm.  Of  course,  it  is  clear  that  the  abnormal 
position  of  the  abdominal  organs — gastroptosis,  en- 
teroptosis,  hepatoptosis — may  act  as  a  predisposing 
factor  by  dragging  upon  the  sensitive  nerve  fibers  of 
the  diaphragm. 


DYSPNCEA   AND   CYANOSIS  1 87 

These  cases  really  belong  to  a  group  of  disturbances 
of  respiration,  attributable  to  reflex  asthma  and  con- 
sequent upon  irritation  of  the  peripheral  nerves. 
Transmission  of  the  irritation  to  the  center  of  respira- 
tion and  to  the  neighboring  vascular  centers  produces 
paroxysmal  dyspnoea  and  a  series  of  vasomotor  mani- 
festations. Considerable  polymorphism  of  the  symp- 
toms results,  and  this  depends  partly  upon  the  per- 
ipheral source  of  irritation,  and  in  part  on  the  tract 
which  the  peripheral  irritation  travels.  Reflex  irri- 
tation of  the  central  apparatus  may  induce  a  continu- 
ous hyperesthesia  of  the  affected  centers,  so  that  the 
latter  will  abnormally  react  tO'  irritations  which  ema- 
nate from  other  parts  of  the  organism. 

HYSTERIA  AND  NEURASTHENIA 

The  polymorphous  forms  of  the  disturbances  of 
respiration,  which  occur  in  hysteria  and  neurasthenia, 
furnish  proof  of  the  condition  described.  If  the  irri- 
tant affects  nerve  fibers,  irritation  of  which  is  capable 
of  inhibiting  respiration,  as  the  superior  laryngeal,  the 
nasal  branches  of  the  trigeminus,  the  branches  of  the 
olfactorius,  glossopharyngeus,  splanchnicus  and  pul- 
monary fibers  of  the  pneumogastric,  dyspnoea  with  re- 
tardation and  deepening  of  respiration  ensues.  In  other 
cases  where  the  accelerator  nerves  of  respiration  are  ir- 
ritated, the  respiratory  movement  will  become  abnor- 
mally frequent  and  superficial.  This  respiratory  neu- 
rosis, called  tachypnoea,  may  be  accompanied  by  tonic 
and  clonic  spasms  of  the  inspiratory  and  expiratory 


1 88      DISORDERS  OF  RESPIRATION  AND  CIRCULATION 

muscles,  and  by  involving  the  vasomotor  center  in  the 
medulla  oblongata  may  produce  manifestations  de- 
pendent upon  the  latter.  Inhibitory  and  exciting  im- 
pulses, however,  may  be  transmitted  to  the  center  of 
respiration  not  only  from  the  periphery,  but  also  from 
the  cerebrum,  from  the  motor  cortical  zones  and  the 
subcortical  centers  of  respiration,  i.  e.,  from  the  cor- 
pora quadrigemina  which  are  connected  with  the  cen- 
ter in  the  oblongata. 

TYPE   OF    HYSTERICAL   DYSPNCEA 

These  physiological  processes  must  be  taken  into 
account  in  the  consideration  of  hysterical  dyspnoea  and 
in  the  explanation  of  the  multiformity  of  its  manifes- 
tations. Nevertheless  there  is  a  definite  type  of  hys- 
terical dyspnoea.  The  hysterical  forms  of  dyspnoea  are 
occasioned  in  many  cases  by  spasms  or  paralysis  of 
the  muscles  of  respiration — glottis  and  diaphragm. 
The  clinical  picture  depends  upon  the  intensity  of  the 
spasm  and  paralysis  as  well  as  on  the  localization.  In 
other  cases,  the  dyspnoea  appears  as  a  central  respira- 
tory neurosis  without  any  mechanical  obstruction  on 
the  part  of  the  muscles  of  respiration.  Diagnostic 
difficulties  are  presented  by  those  cases  where  hysteria 
is  combined  with  organic  lesions  of  the  lung,  heart, 
aorta  and  the  nervous  system,  as  the  accompanying 
hysterical  manifestations  modify  and  complicate  the 
original  affection. 

One  of  the  most  frequent  and  grave  hysterical  af- 
fections is  laryngospasm,  which  may  vary  from  the 


DYSPNCEA   AND   CYANOSIS  189 

slightest  rudimentary  form  of  inspiratory  sigh  to  the 
gravest  type  of  asphyxia.  This  may  even  lead  to 
death,  while  at  autopsy  no  organic  lesion  of  the  in- 
ternal organs  can  be  discovered.  Some  authors  (Land- 
graf,  Lublinski)  describe  a  hysterical  tracheospasm 
caused  by  a  contraction  of  the  smooth  muscular  fibers 
of  the  posterior  tracheal  wall,  which  appears  visible 
by  the  tracheoscope  as  a  prominent  muscular  ridge  un- 
derneath the  mucous  membrane.  In  a  case  reported 
by  Chaput,  dyspnoea  and  stridor  disappeared  after 
catheterizing  the  trachea  and  painting  it  with  cocain. 
The  provocative  factor  may  be  a  laryngeal  catarrh, 
and  the  affection  which  in  itself  is  slight  may  in  chil- 
dren produce  manifestations  of  suffocation  similar 
to  pseudo-croup. 

In  other  cases  there  is  an  hysterical  paralysis  of  the 
posterior  cricoarytenoid  muscle.  The  inspiratory 
dyspnoea,  the  noisy  respiration,  which  can  be  heard  at 
a  distance,  may  in  these  cases  attain  a  high  degree. 
But  even  in  the  majority  of  the  gravest  cases  of 
dyspnoea  there  is  neither  cyanosis  nor  venous  engorge- 
ment. Cases  have  certainly  been  described  where  the 
stormy  stenotic  manifestations  gave  cause  for  resort- 
ing to  tracheotomy.  Expiration  is  unimpeded  and  the 
voice  is,  as  a  rule,  not  changed.  The  laryngeal  crisis 
of  tabes,  the  spasms  of  the  glottis  due  to  foreign  bodies, 
laryngospasm  occurring  in  epileptics  and  the  compres- 
sion of  the  recurrent  laryngeal  in  the  mediastinum  must 
be  differentiated  in  addition  to  affections  of  the  larynx. 

An  interesting  case  of  hysterical  dyspnoea,  described 


190      DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

by  Loubry,  occurred  in  a  man  twenty-seven  years  of 
age.  The  severe  dyspncea  was  characterized  by  deep, 
forced  inspiration  and  labored  expiration,  by  retarda- 
tion of  respirations  which  were  separated  by  long 
pauses  so  that  there  was  a  period  of  apnoea  with  tetanic 
inspiration,  cold  skin  and  anesthesia.  The  periods  of 
apnoea  lasted  from  a  quarter  of  a  minute  to  two 
minutes,  after  w^hich  there  was  a  deep,  noisy  in- 
spiration. The  entire  attack  lasted  about  three- 
quarters  of  an  hour  to  an  hour.  The  periods  of  apnoea 
became  more  frequent  and  lasted  longer;  cyanosis  in- 
creased ;  there  w^as  irregularity  of  the  heart  beat ;  tetanic 
contractions  and  opisthotonus.  Upon  pressure  in  the 
right  iliac  fossa  the  attack  subsided,  after  which  there 
was  sleep,  and  upon  awakening,  normal  breathing. 
There  w^ere,  however,  after  the  awakening,  hysterog- 
enous  areas  below  the  mamillas,  in  the  axilla  and 
in  the  iliac  fossa.  The  attack  w^as  repeated  three 
times  and  was  on  each  occasion  overcome  by  pressure 
upon  the  right  iliac  fossa.  This  case  resembles  the 
pronounced  dyspnoea  of  the  pneumogastric  which 
occurs  in  dogs  after  bilateral  vagotomy,  when  the 
respirations  are  tetanic  and  followed  by  deep,  noisy 
expirations  and  the  intervals  between  the  respirations 
are  protracted.  Respiration  such  as  occurs  in  vagot- 
omized  dogs  has  been  observed  by  Egger  in  a  tabetic 
patient.  The  breathing  was  reduced  to  six  respirations 
per  minute  and  after  several  deep  respirations  there 
were  intervals  in  the  breathing  up  to  ten  seconds. 
A  further  cause  of  dyspnoea  in  hysteria  is  a  func- 


DYSPNCEA   AND   CYANOSIS  I9I 

tional  disturbance  of  the  diaphragm  of  the  nature  of  a 
spasm  and  paralysis.  The  most  frequent  form  is  the 
clonic  diaphragmatic  spasm — singultus  hystericus. 
Though  the  clonic  spasms  are  frequent,  the  tonic 
spasms  of  the  diaphragm  which  lead  to  manifestations 
of  suffocation  and  to  obstruction  of  respiration  even  to 
asphyctic  symptoms  are  inversely  rare.  Fischel  ob- 
served attacks  of  dyspnoea  and  cyanosis  in  consequence 
of  a  tonic  spasm  of  the  diaphragm  on  the  third  day  of 
a  normal  confinement.  Hysterical  paralysis  of  the 
diaphragm  is  equally  rare  and  also  that  form  in  which 
paralysis  of  the  thoracic  muscles  must  be  assumed  and 
where  the  respiratory  movements  occur  exclusively  by 
exaggerated  contractions  of  the  diaphragm.  A  case, 
described  by  Calvare,  a  twenty-five-year-old  woman, 
showed  complete  immobilization  of  the  thorax  and  ex- 
clusively abdominal  breathing. 

One  of  the  most  frequent  disturbances  of  respiration 
in  hysteria  is  hysterical  tachypnoea,  in  which  the  num- 
ber of  respirations  may  be  increased  to  sixty,  one  hun- 
dred or  more  in  a  minute.  Breathing  is  superficial  and 
irregular,  of  the  upper  thoracic  type,  and  with  slight 
participation  or  entire  absence  of  action  of  the  dia- 
phragm. In  spite  of  the  stormy  breathing  and  the 
enormous  acceleration  of  respiration  which  is  accom- 
panied by  marked  gasping — a  picture  which  Erb  has 
compared  to  the  panting  of  chased  and  heated  dogs — ■ 
the  pulse  is  normal  and  the  general  condition  not 
disturbed.  True  dyspnoea  is  absent,  as  is  cyanosis. 
These  attacks  of  tachypnoea  last  a  few  minutes  or 


192      DISORDERS  OF  RESPIRATION  AND   CIRCULATION 

longer,  and  disappear  during  sleep  or  by  distracting  the 
attention.  Other  hysterical  manifestations,  attacks  of 
crying  or  laughing,  may  accompany  the  condition  and 
not  infrequently  it  is  preceded  by  prodromal  signs,  as 
globus  hystericus,  dysphagia,  etc.  Diagnostic  diffi- 
culties can  arise  only  if  hysterical  tachypncea  develops 
in  the  course  of  organic  diseases  of  the  lung  (pneu- 
monia) or  of  the  organs  of  circulation.  This  hap- 
pened in  a  case  of  Weir-Mitchell,  where  a  neurosis 
occurred  after  an  injury  to  the  head  (with  dyspnoeic 
manifestations). 

The  starting  point  of  the  hysterical  disturbances  of 
respiration  is  sometimes,  as  is  well  known,  a  disease  of 
the  genitals.  Odebrecht  cured  a  chronic  spasm  of  the 
diaphragm  in  a  young  woman  by  curetting  the  af- 
fected uterine  membrane,  and  Chrobak  observed  in  a 
hysterical  patient  with  a  retroflexed  uterus,  grave 
spasms  of  respiration  with  threatening  dyspnoea  and 
cyanosis,  which  did  not  return  as  long  as  the  uterus 
was  kept  in  its  normal  position  by  a  pessary. 

DISTURBANCES  OF  RESPIRATION  IN  NEURASTHENIA 

Still  more  complicated  are  disturbances  of  respira- 
tion in  neurasthenia.  Here  symptoms  are  present 
which  must  be  attributed  to  disturbed  function  of  the 
vasomotor  center.  In  the  paroxysms  of  fear,  respira- 
tion is  usually  accelerated  and  snoring,  but  the  dyspnoea 
is  more  subjective.     Cyanosis  is  entirely  absent  if  the 

organs  of  respiration  and  circulation  are  normal.  In 
some  cases,  a  high  position  of  the  diaphragm  is  noted 


DYSPNCEA   AND   CYANOSIS  I93 

in  patients  who  swallow  air  during  the  attacks  and 
thus  distend  the  stomach.  In  these  patients  there  may 
also  be  eructations.  It  is  simply  the  frequency  of  states 
of  anxiety  which  differentiates  neurasthenic  from  hys- 
terical asthma.  Neurasthenic  asthma  interferes  with 
the  patients'  sleep  and  even  awakens  them  when  asleep, 
while  hysterical  asthma  disappears  during  sleep 
(Brugelmann.)  It  is  impossible  in  these  cases  to  give 
general  diagnostic  rules,  because  it  is  just  in  this  field 
of  functional  neurosis  that  combinations  are  so  fre- 
quent which  make  the  pathological  picture  still  more 
varied. 

REFLEX  ASTHMA 

It  has  frequently  been  pointed  out  that  asthma  may 
be  produced  by  reflex  action  from  the  various  organs. 
The  relation  between  nasal  polypi  and  bronchial 
asthma  is  sufficiently  familiar.  There  are  still  to  be 
mentioned  cases  of  asthma  which  occur  when  foreign 
bodies  are  in  the  ear.  In  a  child  observed  by  me, 
dyspncea  disappeared  after  the  removal  of  a  pea  from 
the  ear.  Another  case  is  also  interesting.  A  patient 
living  in  the  country  was  unsuccessfully  treated  by 
physicians  for  asthma.  A  young  physician,  spending 
his  vacations  in  that  section,  remembered  a  clinical  lec- 
ture on  the  subject  of  asthma  verminosum,  and  was 
fortunate  enough  to  think  of  tenia.  He  diagnosed 
the  trouble  correctly  by  examining  the  feces,  and  cured 
the  patient  of  his  asthma  by  an  anthelimintic. 

ORGANIC    CEREBRAL   LESIONS 

Finally,  dyspnoea  may  originate  from  organic  affec- 


T94       DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

tions  affecting-  the  innervation  and  motion  of  the  respir- 
atory apparatus.  The  disturbances  in  breathing  which 
occur  in  cerebral  hemorrhage,  pachymeningitis  and 
meningitis,  are  to  be  looked  upon  as  paralyses  or  dis- 
turbances of  co-ordination.  The  retraction  of  the 
paralyzed  half  of  the  thorax  in  hemiplegia,  especially 
in  deep  inspiration,  and  the  retarded  inspiration  and 
premature  cessation  of  expiration  which  occur  in  other 
cases,  prove  that  respiration  may  be  influenced  by  the 
higher  regions  of  the  brain,  situated  above  the  center 
of  respiration. 

Cheyne-Stokes'  phenomenon  and  similar  intermittent 
disturbances  of  respiration  are  frequently  found  in 
organic  cerebral  lesions,  hemorrhages  and  softening, 
as  well  as  in  uremic  conditions  toward  the  end  of  life. 
In  basilar  meningitis  and  especially  in  tubercular 
meningitis,  there  exist  disturbances  of  co-ordination 
consisting  in  irregular  movements  of  the  respira- 
tory muscles,  chiefly  the  thoracic  muscles  and  the 
diaphragm.  Frequently,  especially  in  the  final  phase 
of  the  disease,  the  respiration  becomes  irregular  and 
accelerated,  and  here  Cheyne-Stokes'  respiratory 
phenomenon  is  obsen^ed  as  a  premortal  sign.  In  all 
these  irregularities  of  respiration,  there  is,  aside  from 
the  stertorous  breathing,  usually  no  true  dyspnoea. 

ORGANIC    SPINAL   LESIONS 

The  condition  is  different  in  direct  lesions  of  the 
center  of  respiration  as  in  atrophy  of  the  nerve  nuclei 
in  bulbar  paralysis.     The  faintness  and  weakness  of 


DYSPNCEA   AND   CYANOSIS  I95 

the  voice,  even  complete  aphony,  owing  to  paralysis  in 
the  area  of  the  recurrent  laryngeal,  as  well  as  the 
dyspnoea  due  to  paralysis  of  the  posterior  crico-ary- 
tenoid  are  well  known.  The  dyspnoea  may  attain  a 
high  degree  where  there  is  weakness  of  the  thoracic 
muscles,  especially  when  a  patient  is  attacked  by 
bronchial  catarrh.  Paroxysms  of  severe  dyspnoea  with 
fright  and  danger  of  suffocation  may  follow  inter- 
ference with  swallowing,  in  consequence  of  paralysis 
of  the  muscles  of  deglutition  allowing  food  to  enter 
the  larynx.  Effects  similar  to  that  in  bulbar  paralysis 
may  also  follow  lesions  of  the  bulbar  nerve  nuclei  in 
other  affections  as  amyotrophic  lateral  sclerosis,  acute 
and  subacute  polyencephalitis,  hemorrhages,  foci  of 
softening  and  tumors  of  the  oblongata  as  well  as 
infantile  paralysis  and  syringomyelia.  The  poly- 
morphous symptom-complex  of  the  laryngeal  crises  of 
tabes,  which  are  accompanied  by  cough,  dysphagia, 
vertigo  and  dyspnoea  on  the  one  hand,  and  fear  and 
sensation  of  suffocation  on  the  other,  belong  in  this 
category  and  are  attributed  to  lesions  of  the  nuclei  of 
the  pneumogastric  and  accessory  nerves.  In  other 
cases  there  is  a  degenerative  neuritis  of  the  pneumo- 
gastric and  recurrent  laryngeal  nerves,  in  which  cases 
paralysis  of  the  laryngeal  muscles,  and  especially  the 
posterior  crico-arytenoid,  may  cause  a  picture  of  the 
most  intense  inspiratory  dyspnoea. 

Affections  of  the  spinal  centers  of  respiration  which 
are  the  origin  of  the  respiratory  nerves  may  lead  to 
dyspnoea  from  paralysis  of  the  respiratory  muscles. 


196        DISORDERS    OF    RESPIRATION"    AND    CIRCULATION 

These  forms  of  paralysis  are  observed  in  affections  of 
the  cervical  region  of  the  cord,  in  caries,  neoplasms,  and 
fractures  of  the  cervical  vertebrse,  in  acute  and  chronic 
myelitis,  in  poliomyelitis  and  amyotrophic  lateral 
sclerosis.  In  the  beginning  of  the  affection,  dyspnoea 
may  be  intermittent  and  may  have  a  spasmodic  char- 
acter like  asthma,  owing  to  irritation  of  the  bulbo- 
medullary  centers.  These  destructive  affections  of  the 
spinal  cord  may  injure  directly  the  spinal  centers  of 
respiration,  and  also  the  tracts  leading  from  the  bulbar 
center  of  respiration  to  the  spinal  centers,  thus  causing 
dyspnoea.  As  the  center  for  the  phrenic  nerve  lies  in 
the  fourth  cervical  segment,  it  is  understandable  why 
paralysis  of  the  diaphragm  is  frequently  observed  to 
occur  in  affections  of  the  spinal  cord  and  meninges 
which  cause  an  Injury  to  the  third  and  fourth  cervical 
roots.  Aside  from  spondylitis,  tumors,  pach5mienin- 
gltls  and  spinal  hemorrhages,  syphilitic  meningeal  af- 
fections especially  lead  to  paralysis  of  the  phrenic 
nerA^e.  In  poliomyelitis,  in  progressive  muscular  atro- 
phy and  in  tabes,  there  may  be  unilateral  or  bilateral 
paresis  and  paralysis  of  the  diaphragm. 

NEURITIS 

In  the  course  of  acute  polyneuritis  of  toxic  or  in- 
fectious origin  (alcohol,  lead,  beri-berl,  diphtheria, 
influenza,  articular  rheumatism,  Landry's  paralysis), 
neuritis  of  the  phrenic  nerve,  may  lead  to  a  paralysis  of 
the  diaphragm^  from  the  extension  of  Inflammatory 
processes  to  the  phrenic  nerve  itself.     The  latter  may 


DYSPNOEA   AND   CYANOSIS  1 97 

happen  after  pleuritis,  pericarditis,  compression  of  the 
nerves  through  indurative  contractions  in  the  apices 
of  the  lungs,  also  by  the  growth  of  neoplasms  in  the 
thoracic  space,  and  finally  in  traumas  as  stab  wounds 
of  the  neck. 

In  paralysis  of  the  diaphragm  there  is  accelerated 
respiration,  but  usually  no  dyspnoea,  during  rest.  But 
with  the  least  exertion,  even  speaking  or  coughing,  the 
dyspnoea  may  reach  an  extreme  degree,  especially  when 
there  are  simultaneous  inflammatory  affections  of  the 
respiratory  system.  On  examination  of  the  patient 
during  quiet  respiration,  there  will  be  found  an  enlarge- 
ment of  the  epigastric  angle  and  a  distention  of  the 
upper  half  of  the  thorax.  On  deep  inspiration  the  cos- 
tal arches  and  epigastrium  will  sink  in,  as  observed  by 
Duchenne,  while  the  upper  half  of  the  chest  is  often  still 
further  distended  with  the  aid  of  the  respiratory  cervi- 
cal muscles  and  atelectatic  rales  may  be  heard  at  the 
margin  of  the  lungs.  Litten's  diaphragmatic  phenome- 
non is  absent  and  the  respiratory  mobility  of  the  lower 
border  of  the  lungs  is  not  demonstrable.  On  the  other 
hand,  the  position  of  the  paralyzed  diaphragm,  even 
during  immobility,  is  high,  shown  also  in  the  Roent- 
gen picture,  and  there  is  aspiration  of  the  abdominal 
organs  into  the  thorax,  and  a  corresponding  tympanitic 
sound  at  the  base  of  the  lung.  Variations  may  be 
present  owing  to  differences  in  degree,  and  as  to 
whether  the  paralysis  is  unilateral  or  bilateral. 

Paralysis  and  atrophy  of  the  intercostal  muscles 
which  occur  frequently  after  polyneuritis,  in  rare  cases 


198        DISORDERS    OF    RESPIRATION    AND    CIRCULATION 

also  in  poliomyelitis,  display  a  behavior  opposite  to 
that  of  diaphragmatic  paralysis.  In  deep  inspiration, 
distention  of  the  upper  half  of  the  thorax  is  absent, 
while  the  action  of  the  diaphragm  causes  a  bulging  of 
the  epigastrium  and  a  retraction  of  the  base  of  the 
thorax. 

The  significance  of  the  pneumogastric  nerve  for  the 
production  of  dyspnoea,  frequently  accompanied  by 
cardiac  manifestations,  has  been  repeatedly  mentioned. 
It  only  remains  now  to  refer  once  more  to  the  degen- 
erative and  neuritic  affections  of  the  pneumogastric 
nuclei  and  trunk,  which  are  partly  primary  and  in  part 
secondary. 

Insufficiency  of  the  diaphragmatic  function  may 
cause  dyspnoea,  possibly  also  cyanosis,  in  the  way  al- 
ready explained  when  speaking  of  trichinosis,  in  pri- 
mary affections  of  the  respiratory  muscles,  as  myositis 
of  the  diaphragm  or  inflammatory  processes,  which 
originate  from  neighboring  organs,  as  diaphragmatic 
pleuritis,  also  not  infrequently  from  suppurative  pro- 
cesses in  the  abdominal  area,  as  subphrenic  abscesses 
consequent  upon  ulcus  ventriculi,  perityphlitis,  exul- 
cerative  carcinoma  of  the  stomach  or  carcinomatous 
infiltration  of  the  lymphatic  vessels  of  the  diaphragm. 

MYOSITIS 

In  acute  hemorrhagic  polymyositis,  in  which  the  en- 
tire transversely  striated  musculature  and  the  subcu- 
taneous tissue  may  be  involved,  simultaneous  and  anal- 


DYSPNCEA   AND    CYANOSIS  199 

ogous  affections  of  the  muscular  substance  of  the  heart 
produce  a  pathological  picture  in  which,  after  preced- 
ing tachycardia  or  arrhythmia,  severe  dyspnoea  and 
fear  with  general  muscular  spasms,  form  the  dommat- 
ing  symptoms. 


IX 

THERAPY  OF  DYSPNCEA 

The  therapy  of  the  various  forms  of  dyspnoea  will 
depend  on  the  nature  of  the  original  affection.  In  the 
cardiac  forms  of  dyspnoea  occasioned  by  valvular  de- 
fects, digitalis  will  be  indicated  in  the  vast  majority  of 
cases,  if  cyanosis  predominates.  When  there  Is  simul- 
taneous anemia  with  hard,  accelerated  pulse,  as  oc- 
curs In  Insufficiency  of  the  aortic  valves  and  especially 
in  the  arteriosclerotic  form,  with  exacerbations  of 
dyspnoea  at  night,  digitalis  will  avail  nothing  or  even 
make  the  condition  worse.  In  such  cases  a  milk  diet, 
In  others  potassium  lodid,  and  finally  preparations 
of  bromid  or  morphln  are  Indicated.  In  dyspnoea, 
caused  by  pulmonary  edema  with  active  hyperemia  of 
the  lungs,  good  service  will  sometimes  be  rendered  by 
local  bleeding,  dry  or  wet  cupping,  moist  packs  to  the 
chest,  counter  Irritant  remedies  like  mustard,  or  local 
mustard  baths  of  hands  or  feet. 

Coincident  renal  insufficiency  requires  caution  in  the 
administration  of  digitalis.  In  disturbances  of  com- 
pensation and  in  degeneration  of  the  cardiac  muscle, 
combinations  of  small  doses  of  digitalis  with  caffein, 
camphor,  ether,  alcohol,  and  In  some  cases  spartein, 
are  many  times  of  benefit.  In  other  cases,  where  there 
is  rapidly  developing  cyanosis  with  dilatation  of  the 


DYSPNCEA   AND    CYANOSIS  20I 

right  ventricle,  bleeding  may  remove  a  threatening 
edema  of  the  lungs,  especially  if  the  symptoms  of  cere- 
bral and  pulmonary  congestion  are  not  benefited  by 
the  cardiac  remedies.  The  same  is  true  of  dyspnoea 
with  grave  cyanosis  in  deformities  of  the  thorax. 

In  effusions  into  the  serous  membranes,  diuretic 
therapy  may  be  employed  (diuretin,  agurin,  theocin), 
and  according  to  circumstances  all  of  the  vegetable 
diuretics  should  be  tried,  as  they  exhibit  considerable 
differences  in  individual  cases.  One  patient  may  react 
to  scilla,  another  to  equisetum  or  ononis ;  even  obsolete 
or  lay  vegetable  remedies  may  be  of  advantage. 

Narcotics  such  as  opium  and  its  derivatives  probably 
cannot  be  entirely  dispensed  with  where  dyspnoea  is 
caused  by  irritation  of  the  cardiac  or  periaortic  plexus, 
or  of  the  pulmonary  fibers  of  the  pneumogastric,  as  in 
dyspnoea  of  bulbar  origin  consequent  upon  ischemia 
of  the  oblongata,  also  in  some  forms  accompanied  by 
attacks  of  stenocardia.  Nitrits,  nitroglycerin,  ery- 
throltetranitrat,  spiritus  setheris  nitrosi,  amylnitrit 
alone  or  in  combination  with  strophanthus  or  even  dig- 
italis, may  in  a  similar  way  relieve  the  patient.  Some 
patients  are  quieted  by  oxycamphor. 

In  the  cardiac  dyspnoea  of  old  persons  with  weak 
hearts,  also  in  the  dyspnoea  of  diseases  of  the  blood, 
arsenic  is  sometimes  effective,  either  alone  or  in  com- 
bination with  digitalis  and  strophanthus.  The  dyspnoea 
of  fatty  heart  in  obese  people  should  be  treated  by 
dietary  measures. 

In  bronchial  asthma,  treatment  with  stramonium, 


202       DISORDERS   OF   RESPIRATION   AND   CIRCULATION 

iodin  preparations  and  morphin  Is  sufficiently  known. 
The  treatment  of  emphysema  of  the  lungs  has  already 
been  described. 

Dyspnoea  in  pneumonia  requires  Individual  treat- 
ment according  to  indications.  Where  there  Is  much 
oppression  with  cyanosis,  dilatation  of  the  cervical 
veins,  abundant  bloody  expectoration,  bleeding  may 
sometimes  be  indicated  in  strong  Individuals ;  In  other 
cases,  cold  packs ;  while  in  still  others,  amylnltrit  may 
do  well. 

The  treatment  of  dyspnoea  in  phthisis  depends  upon 
Its  cause.  Indications  will  differ  In  pneumothorax, 
febrile  dyspnoea  and  in  the  simultaneous  Involvement 
of  the  heart  and  pericardium. 

In  bronchitis  with  scant  expectoration,  expectorants 
like  ipecac,  senega  and  antimony  may  become  neces- 
sary. In  diphtheria  antitoxin  treatment,  emetics.  In- 
tubation or  tracheotomy,  in  edema  of  the  glottis  cup- 
ping, leeches  to  the  neck,  drastic  purgation  or  surgical 
interference. 

For  the  treatment  of  renal  dyspnoea,  no  general  rules 
can  be  established.  There  are  cases  in  which  an  ex- 
clusive milk  diet  alleviates  the  symptoms.  In  others 
theobromin  preparations,  and  In  still  others,  diuretics 
and  drastic  remedies,  ether  In  large  doses,  even  bleed- 
ing, morphin  Injections,  and  In  some  cases  lumbar 
puncture.  In  diabetic  acid  dyspnoea,  large  doses  of 
soda  bicarbonat  should  be  tried,  also  Intravenous  In- 
jections of  the  same,  which,  however,  are  nearly  always 
•useless. 


DYSPNCEA    AND    CYANOSIS  2O3 

Inhalations  of  oxygen  in  the  treatment  of  dyspnoeic 
conditions  in  various  affections  enjoy  a  certain  reputa- 
tion. In  carbonmonoxid  intoxications,  in  which  the 
tissues  are  insufficiently  supplied  with  oxygen  in  con- 
sequence of  the  formation  of  carbonmonoxidhemo- 
globin,  also  in  intoxications  with  agents  which  form 
methemoglobin,  oxygen  therapy  both  in  the  form  of 
inhalations  and  by  rectal  administration  is  advisable 
and  theoretically  well  founded. 

A  further  indication  for  oxygen  is  morphin  poison- 
ing. We  have,  ourselves,  seen  a  grave  case  of  mor- 
phin poisoning  which  was  saved  by  tracheotomy  and 
artifical  respiration,  with  pure  oxygen  administered 
through  the  tracheal  canula. 

In  other  forms  of  dyspnoea  of  mechanical  origin,  as 
in  stenosis  of  the  upper  air  tract,  emphysema,  cardiac 
asthma,  dyspnoea  in  phthisis,  also  in  pneumonia,  in 
affections  of  the  blood,  as  pernicious  anema  and  leu- 
kemia, there  are  often  cases  in  which  inhalations  of 
oxygen  give  the  patients  at  least  some  alleviation  of 
the  subjective  difficulty  in  breathing. 


0    DISORDERS  OF    a 

s 

M?„£l?h°'by  Prof.  Dr.  CARL  von  NOORDEN 

Physician-in-Chief  to  the  City  Hospital,  Frankfort-on-Main 

Authorized  American  Edition  ^"^"'^^'^££0';  '■^^.^!^¥'n^^Lfn^t^^^^^ 

T  is  due  to  the  disorders  of  metabolism  and  nutrition  that  degenerative  changes 
cut  short  the  activities  of  so  many  men  and  women  in  middle  life, — that,  in 
these  latter  days,  senility  and  death  itself  come  prematurely  to  a  very  large  pro- 
portion of  mankind.  Such  disorders  constitute  the  bane  of  our  modern  civilization. 
They  have  been  in  some  measure  also  a  reproach  to  the  science  and  art  of  medicine, 
since  until  very  recently  they  have  not  been  studied  with  a  thoroughness  com- 
mensurate with  their  importance. 

I.  OBE.SITY,  THE  INDICATIONS  FOR  REDUCTION 
CURES. — In  this  volume  the  disease  is  considered  in  a  manner  which  is  at 
once  scientific  and  practical;  based  upon  exhaustive  experiments  and  bedside 
observations  carried  on  under  the  direction  of  the  author. 

Cloth,  8vo,  60  pages,  50  cents. 

II.  NErPHRITIS.— The  author's  handling  of  this  subject  is  varied  and 
original,  and  in  various  respects  he  has  established  for  the  treatment  of  the  different 
forms  of  Bright's  disease,  rules  founded  upon  a  critical,  scientific  study  of  numerous 
cases  instead  of  the  familiar  directions  handed  down  from  an  earlier  period. 

Cloth,  8vo,  112  p&ges,  $1.00. 

III.  COLITIS. — The  author  covers  the  complex  subject  of  Membranous 
Catarrh  of  the  Intestines  {Colica  Mucosa),  in  a  manner  which  is  well-nigh  ex- 
haustive and  also  most  convincing  since  he  is  able  to  report  a  remarkably  large 
proportion  of  cures  obtained  by  the  method  which  he  recommends. 

Cloth,  @vo,  64  pages,  50  cents. 

IV.  THE  ACID  AUTOINTOXICATIONS.— These  studies  into 
the  derangements  of  metabolism,  which  result  in  an  overproduction  of  acid, 
concern  the  clinician  very  nearly.  They  are  in  a  field  which  has  been  hitherto 
too  little  explored.  Cloth,  8vo,  80  pages,  50  cents. 

V.  SALINE,  THERAPY.— The  author  here  decides  many  mooted  ques- 
tions concerning  the  influence  of  the  sodium  chloride  waters  on  the  digestion,  as 
well  as  in  gout,  diabetes  and  other  diseases  of  nutrition. 

Cloth,  8vo,  96  pages,  75  cents. 

VI.  DRINK  RESTRICTION.  (Thirst  Cures)— A  most  instructive 
deliverance  upon  a  subject  of  the  highest  practical  importance. 

Cloth,  Sv^o,  90  pages,  75  cents. 

VII.  DIABETES  MELLITUS,  A  Series  of  Lectures  delivered  before 
the  University  and  Bellevue  Hospital  IVledical  College,  New  York.    Oct.,  1905. 

Cloth,  8vo,  212  pages,  $1.50. 

VIII.  GOUT.     In  Press. 


E.  B.  TREAT  &  CO.,  Publishers,  ^^"  ""'-^ew^ork''  '*"'* 


DISEASES 


OF   THE 

Stomach  and  Intestines 

As  well  as  the  Allied  and  Resultant  Conditions,  with 
Modern  Methods  of  Diagnosis  and  Treatment 

By   BOARDMAN    REED,    M.D. 

THE  AUTHOR  has  had  large  experience  in  this  special  field 
of  medicine,  supplemented  by  knowledge  acquired  during 
twenty  years  spent  in  a  busy  general  practice  among  chronic 
invalids  in  Atlantic  City,  postgraduate  work  both  in  this  country 
and  abroad,  and  teaching  in  this  special  department,  and  is 
eminently  qualified  for  the  task  he  has  so  successfully  completed. 

THE  VOLUME  covers  so  comprehensively  the  etiology,  path- 
ology, symptomatology,  diagnosis  and  treatment  of  the  various 
diseases  in  question  that  it  stands  as  the  only  thoroughly  up-to- 
date  single  volume  work  on  the  diseases  of  the  stomach  and  in- 
testines. The  instruction  is  so  plain  and  simple  that  every 
general  practitioner,  as  well  specialists  in  other  lines,  will  tind 
it  a  real  help  in  the  countless  puzzHng  cases  complicated  with,  or 
wholly  dependent  upon,  derangements  in  the  digestive  system. 

SPECIAL  FEATURES  are  "The  Gastrointestinal  Clinic"  in 
which  the  diagnosis  and  treatment  of  all  known  diseases  of  the 
tract  are  separately  considered;  a  very  complete  "  Symptomatic 
Guide  to  Diagnosis";  an  account  of  the  relations  of  gastroin- 
testinal diseases  to  numerous  other  affections,  such  as  Neuras- 
thenia, Insomnia,  Heart  Disease,  Kidney  Disease,  etc.,  and  a 
comprehensive  account  of  the  diagnosis  and  treatment  of 
Diseases  of  the  Rectum  and  Anus  contributed  by  Dr.  Collier 
F.  Martin,  the  well-known  specialist. 


"The  author  is  clear  and  sound  in  his 
teaching's,  simplifies  conditions  as  far  as  pos- 
sible, and  gives  a  good  practical  working 
knowledge,  such  as  he  has  gathered  from  a 
large  experience  in  this  speciallield." — Medi- 
cal Record. 


''  The  need  of  a  modern  treatise  on  thii? 
subject  is  evident  from  the  limited  literature 
and  increasing  demand  for  the  same.  Not 
only  general  practitioners,  but  also  special 
ists  in  other  lines,  will  find  it  of  great  value." 
— A  merican  Medicine. 


Complete  in  One  Large  Octavo  Volume;    1024  pages. 
Profusely  Illustrated.    Half  Morocco,  $6.00.    Cloth,  $5.00 

Sent  Post  or  Express  Paid  on  receipt  of  Price.     Circulars  upon  request 

E.  B.  TREAT  6  CO.,  Publishers 
241'243  West  TWenty^Third  Street,   Neb)  York 


OPERATION 


-IN- 


Diseases  of  the  Internal  Organs 

By  PROF.  HERMANN  SCHLESINGER,  Vienna 

AUTHORIZED  ENGLISH  TRANSLATION 

By  K.  W.  MONSARRAT,  F.R.C.S.  Ed.,  Surgeon  Noithern   Hospital,  Liverpool 


From  the  Author's  Preface—"  I  have  written  essentially  for 
the  practitioner.  I  have,  therefore,  avoided  all  prolix  discus- 
sion, and  confined  myself  to  the  consideration  of  the  questions 
indicated  by  the  special  design  of  the  work.  On  the  advice  of 
colleagues  whom  I  have  consulted,  I  have  included  in  each 
chapter  some  remarks  on  etiology,  pathological  anatomy,  clinical 
course,  diagnosis  and  differential  diagnosis,  with  a  view  to 
enabling  the  practitioner  to  quickly  obtain  a  general  grasp  of 
the  condition  under  consideration.  These  paragraphs,  are, 
however,  subordinate  to  the  main  purpose  of  my  undertaking — 
that  of  enabling  medical  men  who  are  not  in  hospital  practice 
to  arrive  at  an  independent  opinion  on  the  advisability  of  opera- 
tion in  a  large  majority  of  cases  of  internal  lesion.  This  is  not 
a  mere  compilation.  Many  years'  work  in  hospital  and  private 
practice  have  given  me  the  opportunity  of  acquiring  a  large 
experience  in  the  questions  here  discussed." 


American  Journal   of   Surgery,   New 

York,  says:  "We  do  not  recall  that  this 
subject  has  ever  been  touched  upon  in  a 
separate  volume  before,  or  even  adequately 
in  volumes  devoted  to  collective  discus- 
sions. This  work  may  therefore  be  said  to 
fill  a  definite  want.  It  is  novel  in  another 
respect,  namely,  that  a  presumably  surgical 
subject  is  discussed  by  a  medical  man. 
This  feature,  we  believe,  adds  greatly  to 
the  value  of  the  book,  inasmuch  as  it  intro- 
duces a  point  of  view  that  is  only  too 
frequently  wanting." 


riedical  Standard,  Chicago,  says:  "A 
most  timely  and  distinctively  purposeful 
work.  Of  all  the  problems  which  the  wide- 
sweeping  activities  of  operative  surgery 
have  imposed  upon  the  general  practi- 
tioner, the  question  of  when  to  operate 
and  when  not  to,  is  the  most  difficult  and 
delicate.  A  guide  to  the  solution  of  this 
hydra-headed  problem,  therefore,  and  from 
an  authority  so  universally  recognized  as 
Dr.  Schlesinger,  cannot  fail  to  be  peculiarly 
welcome.  All  will  do  well  to  read,  mark, 
learn,  and  inwardly  digest." 


One  Volume,  8vo,  (8^  x  5K  inches),  514  pages,  doth,  net,  $3.00 


E.  B.  TREAT  &  CO.,  241-243  W.  23d  Su,  New  York 


MEDICAL    AND    SUKGICAL 

USES     OF 

ILLUCTRICIT 

INCLUDING 

X-Ray  and  Vibratory  Therapeutics,  the  Finsen  Light  and 
High  Frequency  Currents 

BY 

A.  D.  ROCKWELL,  A.M.,  M.D. 

Formerly  Professor  of  Electro-Therapeutics  in  the  N,  Y.  Post-Graduate  Medical  School  ana 

Hospital:  Fellow  of  the  New  York  Academy  of  Medicine  ;  Member  of  the  Atneri 

can  Academy  of  Medicine :    Member  of  the  New    York  Neurological 

Society:    Forjnerly    Electro-Therapeutist    to  the    VVo/nan''s 

Hospital  in  the  State  of  New  York,  etc. 

Electricity  in  its  relation  to  medical  science,  as  well  as  to  commerce, 
has  made  wonderful  progress  in  recent  years.  The  recognized  pioneer 
work  in  America  was  the  treatise  on  *'  The  Medical  and  Surgical  Uses  cf 
Electricity,"  byBeard  and  Rockwell,  of  which  eight  successive  editions  were 
issued.  In  1896  the  stereotype  plates  were  destroyed  and  the  work  re- 
written by  Dr.  Rockwell,  and  issued  from  an  entirely  new  set  of  plates.  To 
keep  abreast  of  the  marvelous  progress  in  this  department  of  Medicine,  a 
New  Edition  is  again  offered  to  the  profession.  The  Roentgen  X-Ray  in  its 
relation  to  Diagnosis  and  Therapeutics  has  been  entirely  rewritten.  Other 
additions  include  the  subject  of  the  Actinic  Rays  of  light  (Finsen's),  High 
Frequency  Currents  and  Vibratory  Therapeutics.  In  the  body  of  the  book 
much  that  has  served  its  purpose  has  been  discarded  and  new  and  up-to- 
date  material  substituted.  It  is  confidently  believed  that  in  its  pages  will 
be  found  a  comprehensive  and  accurate  survey  of  this  fascinating  and 
growing  field  of  research. 


Medical  Record,  New  York,  says:  "For 
twenty  years  and  more  the  work  of  Beard  and 
Rockwell  has  been  the  leading  authority  in 
this  country  on  the  subject  which  it  treats. 
They  were  the  pioneers  in  the  field  of  elec- 
tro-therapeutics and  enunciated  ideas  and 
methods  which  have  stood  the  test  of  time.  . 
The  work  plainly  sets  forth  all  the  fun- 
damental principles  of  electricity,  and  in  its 
relation  to  disease  is  clear  in  detail  and  can- 
not fail  to  greatly  aid  all  who  are  interested 
in  this  department  of  medical  science." 


Medical  News,  Philadelphia,  says  :  "The 
methods  of  application  for  therapeutic  pur- 
poses are  given  in  detail  and  with  such  clear- 
ness that  the  general  practitioner  will  find  the 
book  a  useful  and  practical  guide.  ' 

Medical  Journal,  New  York,  says:  "The 
book  is  much  changed  from  the  earlier  edi- 
tions, being  in  accord  with  the  advance  in 
our  knowledge  of  the  applications  of  electri- 
city. .  .  .  The  work  is  valuable  and  wil' 
clear  up  many  points  which  may  be  shadowy 
in  the  mind  of  the  general  practitioner." 


New,    Revised  and  Enlarged  Edition, 

Royal  Octavo,  692  pages;  Illustrated. 

Cloth,  $5.00  net.  Half  Morocco,  $6.00,  net. 


E..  B.  TREIAT   <S    CO.,  Publishers 

24^-243  West  23d  Street.  New  York 


